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Relevant bibliographies by topics / Drug resistance in microorgani

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Academic literature on the topic 'Drug resistance in microorgani'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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Journal articles on the topic "Drug resistance in microorgani"

1

Greenlees, Kevin J. "Animal Drug Human Food Safety Toxicology and Antimicrobial Resistance—The Square Peg." International Journal of Toxicology 22, no. 2 (March 2003): 131–34. http://dx.doi.org/10.1080/10915810305091.

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This paper presents the traditional approach for the evaluation of human food safety used for animal drugs intended for food animals, and describes some of the difficulties posed by antimicrobial drug resistance. Like human drugs, animal drugs must be safe and effective for the patient. However, unlike human drugs, food derived from animals treated with the animal drug must also be shown to be safe for human consumption. The Food and Drug Administration has come to realize that antimicrobial drugs used in the treatment of the food animal have the potential to create a unique residue—increased numbers of microorganism that are resistant to antimicrobial drug treatment. The traditional toxicological paradigm for chemical residues does not apply to this unique microbiological residue. Information useful to a food safety evaluation may include the potential for the animal antimicrobial drug to diminish the susceptibility of microorganisms to human antimicrobial drugs, any human medical use of the drug, relationship to other human antimicrobial drugs, and the ability of the animal drug to alter the susceptibility of relevant microorganism to important human antimicrobial drugs. Yet to be developed are standardized approaches to quantify an acceptable level of resistant microorganism in food and to mitigate the hazard to assure that there is a reasonable certainty of no harm following the consumption of the edible food derived from the treated animal.

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VIANNA, Júlia Silveira, Ivy Bastos RAMIS, Daniela Fernandes RAMOS, Andrea VON GROLL, and Pedro Eduardo Almeida da SILVA. "DRUG RESISTANCE IN HELICOBACTER PYLORI." Arquivos de Gastroenterologia 53, no. 4 (December 2016): 215–23. http://dx.doi.org/10.1590/s0004-28032016000400002.

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ABSTRACT Background Helicobacter pylori has a worldwide distribution and is associated with the pathogenesis of various diseases of the digestive system. Treatment to eradicate this microorganism involves the use of a combination of antimicrobials, such as amoxicillin, metronidazole, clarithromycin, and levofloxacin, combined with proton pump inhibitors. Although the current therapy is effective, a high rate of treatment failure has been observed, mainly because of the acquisition of point mutations, one of the major resistance mechanisms developed by H. pylori. This phenomenon is related to frequent and/or inappropriate use of antibiotics. Conclusion This review reported an overview of the resistance to the main drugs used in the treatment of H. pylori, confirming the hypothesis that antibacterial resistance is a highly local phenomenon and genetic characteristics of a given population can influence which therapy is the most appropriate.

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Gudata, Daba, and Feyissa Begna. "ANTIMICROBIAL RESISTANCE: REVIEW." International Journal of Research -GRANTHAALAYAH 6, no. 11 (November 30, 2018): 77–93. http://dx.doi.org/10.29121/granthaalayah.v6.i11.2018.1091.

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Antimicrobial resistance (AMR) is resistance of a microorganism to an antimicrobial that was originally effective for treatment of infections caused by it. Increasing clinical incidence of antimicrobial resistance is a major global health care issue and the situation is perhaps aggravated in developing countries. Although, AMR is a major health care issue, there is a shortage of documented information on it. Therefore, the aim of this paper is to review the causes or risk factors, problems, mechanisms and control of antimicrobial resistance. The resistance problem can be seen simplistically as an equation with two main components: the antibiotic or antimicrobial drug, which inhibits susceptible organisms and selects the resistant ones; and the genetic resistance determinant in microorganisms selected by the antimicrobial drug. Antimicrobial resistance is associated with high mortality rates and high medical costs and has a significant impact on the effectiveness of antimicrobial agents. To appreciate the mechanisms of antimicrobial resistance, it is important to understand how antimicrobial agents act. The resistance mechanisms therefore depend on which specific pathways are inhibited by the drugs and the alternative ways available for those pathways that the organisms can modify to get a way around in order to survive. A comprehensive strategy is necessary to address the challenges that accompany the rising threat of antimicrobial resistance. Special vigilance must now be paid to appropriate selection and timing of antimicrobial agents as a major force in reducing the development of antimicrobial resistance. Prevention and control of these infections will require new antimicrobial agents, prudent use of existing agents, new vaccines, and enhanced public health efforts to reduce transmission.

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Pontes, Daniela Santos, Rodrigo Santos Aquino de Araujo, Natalina Dantas, Luciana Scotti, Marcus Tullius Scotti, Ricardo Olimpio de Moura, and Francisco Jaime Bezerra Mendonca-Junior. "Genetic Mechanisms of Antibiotic Resistance and the Role of Antibiotic Adjuvants." Current Topics in Medicinal Chemistry 18, no. 1 (March 22, 2018): 42–74. http://dx.doi.org/10.2174/1568026618666180206095224.

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The ever increasing number of multidrug-resistant microorganism pathogens has become a great and global public health threat. Antibiotic mechanisms of action and the opposing mechanisms of resistance are intimately associated, but comprehension of the biochemical and molecular functions of such drugs is not a simple exercise. Both the environment, and genetic settings contribute to alterations in phenotypic resistance (natural bacterial evolution), and make it difficult to control the emergence and impacts of antibiotic resistance. Under such circumstances, comprehension of how bacteria develop and/or acquire antibiotic resistance genes (ARG) has a critical role in developing propositions to fight against these superbugs, and to search for new drugs. In this review, we present and discuss both general information and examples of common genetic and molecular mechanisms related to antibiotic resistance, as well as how the expression and interactions of ARGs are important to drug resistance. At the same time, we focus on the recent achievements in the search for antibiotic adjuvants, which help combat antibiotic resistance through deactivation of bacterial mechanisms of action such as β-lactamases. Recent advances involving the use of anti-resistance drugs such as: efflux pump inhibitors; anti-virulence drugs; drugs against quorum sensing; and against type II/III secretion systems are revealed. Such antibiotic adjuvants (as explored herein) collaborate against the problems of antibiotic resistance, and may restore or prolong the therapeutic activity of known antibiotics.

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Ahmad, Ijaz, Lingli Huang, Haihong Hao, Pascal Sanders, and Zonghui Yuan. "Application of PK/PD Modeling in Veterinary Field: Dose Optimization and Drug Resistance Prediction." BioMed Research International 2016 (2016): 1–12. http://dx.doi.org/10.1155/2016/5465678.

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Among veterinary drugs, antibiotics are frequently used. The true mean of antibiotic treatment is to administer dose of drug that will have enough high possibility of attaining the preferred curative effect, with adequately low chance of concentration associated toxicity. Rising of antibacterial resistance and lack of novel antibiotic is a global crisis; therefore there is an urgent need to overcome this problem. Inappropriate antibiotic selection, group treatment, and suboptimal dosing are mostly responsible for the mentioned problem. One approach to minimizing the antibacterial resistance is to optimize the dosage regimen. PK/PD model is important realm to be used for that purpose from several years. PK/PD model describes the relationship between drug potency, microorganism exposed to drug, and the effect observed. Proper use of the most modern PK/PD modeling approaches in veterinary medicine can optimize the dosage for patient, which in turn reduce toxicity and reduce the emergence of resistance. The aim of this review is to look at the existing state and application of PK/PD in veterinary medicine based onin vitro,in vivo, healthy, and disease model.

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Kumar, Rajiv, Akhilesh Kumar, Umashanker Prasad Keshri, Manju Gari, Sumit Kumar Mahato, and Pholgu Protim. "Antimicrobial susceptibility pattern of pus culture in a tertiary care hospital of Jharkhand, India." International Journal of Basic & Clinical Pharmacology 6, no. 5 (April 24, 2017): 1184. http://dx.doi.org/10.18203/2319-2003.ijbcp20171674.

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Background: Antimicrobial resistance is developing day by day leading to increase not only in health care cost but also severity and death rate from certain infection that could have been avoided by rational use of existing and new antimicrobial agents. Present study is undertaken for this purpose to analyse the types of pathogens involved and their antibiotic sensitivity isolated from pus culture reports in a tertiary care hospital.Methods: Observational study was conducted using pus culture and sensitivity reports collected retrospectively from the records maintained in the Department of Microbiology over a period of 5 months from August 2016 to December 2016 in tertiary care hospital.Results: 85 percent pus samples were found culture positive of which microorganism isolated in decreasing order were Staphylococcus aureus, Pseudomonas, Klebsella and E. coli. Staphylococcus aureus was sensitive to fixed drug combination of piperacillin with tazobactam, linezolid, ceftriaxone with sulbactum, levofloxacillin and ciprofloxacin and resistance to cefotaxime, cloxacillin and ampicillin. Pseudomonas was highly sensitive to fixed drug combination of cefoperazone with sulbactum, piperacillin with tazobactum, ceftriaxone with sulbactum and resistance to cloxacillin and cefotaxime. Klebsiella showed high sensitivity to piperacillin with tazobactum, cefoperazone with sulbactum, ceftriaxone with sulbactum and was found resistant with norfloxacin and amoxycillin. E. coli showed high sensitivity in decreasing order with amikacin and gentamycin and resistance in increasing order with cefotaxime, cloxacillin, ampicillin and norfloxacin.Conclusions: The sensitivity patterns were different for each isolated microorganism but high sensitivity was found with fixed antimicrobial drug combination and resistance to frequently used drugs.

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Miller, M. A. "Quality control and safety of animal products." Canadian Journal of Animal Science 79, no. 4 (December 1, 1999): 533–38. http://dx.doi.org/10.4141/a99-010.

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This paper discusses the new animal drug approval process regulated by the Center for Veterinary Medicine (CVM), Food and Drug Administration (FDA) of the United States. The Center for Veterinary Medicine of FDA considers two criteria in ensuring the human food safety of edible animal products: i) safety of the chemical residues and ii) for antimicrobial products, microbiological safety including changes in bacterial pathogen load and resistance pattern. The hazard associated with animal drug products of non-carcinogenic compounds is assessed by conducting a standard battery of toxicology test, whereas the hazard from the carcinogenic potential of compounds is evaluated based on structure, results of genetic toxicity tests, and toxicology studies. Post approval monitoring is carried out to ensure that the animal drugs are being used properly after their approval. Particular concern is given to those eliciting an "acute" toxic reaction at relatively low levels. The other aspect of food safety regulated by CVM of FDA is microbiological safety, especially to antimicrobial drugs used at subtherapeutic levels in feeds. The studies are designed by FDA to ensure that antibiotic treatment of food-producing animals does not alter pathogen load or resistance pattern of pathogens. Two studies are generally performed: i) the salmonella shedding study, which addresses the effect of drug treatment on the excretion of salmonella in the feces of animals artificially infected with salmonella; and ii) the coliform resistance study, which monitors the effect of the drug on the resistance pattern of E. coli present in the endogenous fecal flora. After a retrospective study of the microbiological safety over past 20 yr, CVM of FDA is planning to revise some microbiological safety studies with focuses on: i) pathogen load, pathogen excretion and microorganism resistance pattern at the time of slaughter; and ii) susceptibility studies on products that have utility in human medicine. Key words: Animal drug, food safety, antibiotic

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Ugwu, D. I., B. E. Ezema, F. U. Eze, and D. I. Ugwuja. "Synthesis and Structural Activity Relationship Study of Antitubercular Carboxamides." International Journal of Medicinal Chemistry 2014 (December 30, 2014): 1–18. http://dx.doi.org/10.1155/2014/614808.

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The unusual structure and chemical composition of the mycobacterial cell wall, the tedious duration of therapy, and resistance developed by the microorganism have made the recurrence of the disease multidrug resistance and extensive or extreme drug resistance. The prevalence of tuberculosis in synergy with HIV/AIDS epidemic augments the risk of developing the disease by 100-fold. The need to synthesize new drugs that will shorten the total duration of effective treatment and/or significantly reduce the dosage taken under DOTS supervision, improve on the treatment of multidrug-resistant tuberculosis which defies the treatment with isoniazid and rifampicin, and provide effective treatment for latent TB infections which is essential for eliminating tuberculosis prompted this review. In this review, we considered the synthesis and structure activity relationship study of carboxamide derivatives with antitubercular potential.

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Thompson, Dorothea K., and Stephen M. Sharkady. "Genomic Insights into Drug Resistance Determinants in Cedecea neteri, A Rare Opportunistic Pathogen." Microorganisms 9, no. 8 (August 15, 2021): 1741. http://dx.doi.org/10.3390/microorganisms9081741.

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Cedecea, a genus in the Enterobacteriaceae family, includes several opportunistic pathogens reported to cause an array of sporadic acute infections, most notably of the lung and bloodstream. One species, Cedecea neteri, is associated with cases of bacteremia in immunocompromised hosts and has documented resistance to different antibiotics, including β-lactams and colistin. Despite the potential to inflict serious infections, knowledge about drug resistance determinants in Cedecea is limited. In this study, we utilized whole-genome sequence data available for three environmental strains (SSMD04, M006, ND14a) of C. neteri and various bioinformatics tools to analyze drug resistance genes in this bacterium. All three genomes harbor multiple chromosome-encoded β-lactamase genes. A deeper analysis of β-lactamase genes in SSMD04 revealed four metallo-β-lactamases, a novel variant, and a CMY/ACT-type AmpC putatively regulated by a divergently transcribed AmpR. Homologs of known resistance-nodulation-cell division (RND)-type multidrug efflux pumps such as OqxB, AcrB, AcrD, and MdtBC were also identified. Genomic island prediction for SSMD04 indicated that tolC, involved in drug and toxin export across the outer membrane of Gram-negative bacteria, was acquired by a transposase-mediated genetic transfer mechanism. Our study provides new insights into drug resistance mechanisms of an environmental microorganism capable of behaving as a clinically relevant opportunistic pathogen.

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Popovici, Sonia Elena, Ovidiu Horea Bedreag, and Dorel Sandesc. "Evolution of Acinetobacter baumannii infections and antimicrobial resistance. A review." Central European Journal of Clinical Research 2, no. 1 (April 1, 2019): 28–36. http://dx.doi.org/10.2478/cejcr-2019-0005.

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AbstractThe emergence of multi-drug resistantAcinetobacter sppinvolved in hospital-acquired infections, once considered an easily treatable pathogen, is troublesome and an immense burden for the modern medical systems worldwide. In the last 20 years the medical community recorded an increase in the incidence and severity of these infections as therapeutic means tend to be less and less effective on these strains. The ability of these bacteria to rapidly develop resistance to antimicrobial agents by continuously changing and adapting their mechanisms, their ability to survive for long periods of time in the hospital environment and the multitude of transmission possibilities raises serious issues regarding the management of these complex infections. The future lies in developing new and targeted methods for the early diagnosis ofA. baumannii, as well as in the judicious use of antimicrobial drugs. This review details the evolution of the pathogenicity of this microorganism, together with the changes that appeared in resistance mechanisms and the advancements in molecular testing for the early detection of infection.

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Dissertations / Theses on the topic "Drug resistance in microorgani"

1

Abate, Getahun. "Drug resistance in mycobacterium tuberculosis /." Stockholm, 1999. http://diss.kib.ki.se/1999/91-628-3833-4/.

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Marijani, Theresia. "Modelling drug resistance in malaria." Thesis, Stellenbosch : University of Stellenbosch, 2009. http://hdl.handle.net/10019.1/4063.

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Abrahem, Abrahem F. "Mechanisms of drug resistance in malaria." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape7/PQDD_0033/MQ50704.pdf.

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Scott, F. M. "Drug resistance mechanisms in multiple myeloma." Thesis, University of Edinburgh, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.661665.

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The aim of this thesis was to investigate expression of putative drug resistance markers in myeloma both by examining clinical material and through the development of a xenograft model. Pgp expression was examined in 57 samples from 37 patients with myeloma. Of 23 samples at presentation and 37 at relapse, 7 and 26 respectively were Pgp positive. A myeloma xenograft model was established to examine the acute effects of cytotoxic drugs on the expression of "classical" drug resistance markers and genes involved in regulation of apoptosis. The untreated xenografts were Pgp negative, expressed low levels of glutathione S-transferase-P (GSTP) and had readily detectable topo I and II. Little p62 myc or p53 were detected, whereas bcl-2 was strongly expressed. Treated xenografts contained only scattered apoptotic cells, but the majority demonstrated cell cycle arrest at the G2/M transition, and GSTP and topo IIα expression were increased. Pgp expression was also increased in animals treated on 3 consecutive days. C-myc was detected in dead or dying cells, but there was no mutational inactivation of p53, and bcl-2 expression was unaltered. The increased Pgp and GSTP expression following therapy, rather than inducing a resistant phenotype, may reflect activation of expression by drug administration. Cellular resistance occurred despite evidence of DNA damage suggesting that resistance arose from failure to engage apoptosis, possibly due to the strong bcl-2 expression. Bcl-2 expression was therefore evaluated in 40 samples from 31 individuals, with strong expression observed in over 80% of cases. This was not associated with rearrangement of the bcl-2 locus. The presence of abundant bcl-2 protein in the majority of cases has potentially important implications for drug resistance in this disease and suggests that future assessment of drug resistance in myeloma may be better directed downstream of immediate drug-target interactions to regulation of engagement of apoptosis.

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Wildridge, David. "Metabolism and drug resistance in Trypanosomatids." Thesis, University of Glasgow, 2012. http://theses.gla.ac.uk/3622/.

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The principle aim of this project is the investigation of metabolism and mechanisms of pentamidine resistance in trypanosomatids. An understanding of these mechanisms may allow the development of novel drugs to treat Leishmaniasis and human African trypanosomiasis (HAT), caused by the protozoan parasites Leishmania spp and Trypanosoma brucei. In this study a pentamidine resistance L. mexicana promastigote cell line was generated in vitro. This cell line was 20-fold resistant to pentamidine when compared to the parental wild type cells. Furthermore, these lines were cross resistant to other diamidine compounds. A proteomic analysis of these cell lines revealed numerous changes to the proteome, with the down regulation of several flagellar proteins. A hypothesis to investigate a role of the voltage dependent anion channel (VDAC) in pentamidine resistance was also explored. The metabolomic approach involved the investigation of transketolase and the pentose phosphate pawthway. A previous study involving a transketolase knockout T. brucei cell line indicated that an increased sensitivity to pentamidine and methylene blue. A transketolase deficient L. mexicana cell line was generated to test this hypothesis in Leishmania, however the differences were minimal. A metabolomic analysis of the L. mexicana tkt null cell line (lmtkt-/-) revealed an increase in ribose 5-phosphate, a key substrate of transketolase. Erythrose 4-phosphate also increased in the lmtkt-/- cells, indicating a source of this metabolite independent of TKT. It appears that the deletion of TKT prevents any flux through the oxidative branch of the PPP returning to the glycolytic pathway. Interestingly, the lmtkt-/- cells do not acidify the medium to the same extent as the wild type cells; however a glucose assay indicated that both cell lines used similar quantities of glucose. This would suggest that there is a change in the metabolites excreted by the lmtkt-/- cell line. Finally, a global metabolomics approach was investigated using high resolution mass spectrometry. Metabolomics is a rapidly developing field in systems biology, and whilst significant improvements have been made in mass spectrometry; the ability to analyse and interpret raw metabolomic datasets on a global scale has been largely neglected. Consequently, a database program to query these complex datasets was constructed.

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Pongtavornpinyo, Wirichada. "Mathematical modelling of antimalarial drug resistance." Thesis, University of Liverpool, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.428249.

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Doherty, Catherine Jean. "Drug resistance mechanisms in multiple myeloma." Thesis, University of Edinburgh, 1997. http://hdl.handle.net/1842/22154.

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Galinytė, Daiva. "Antibiotikų vartojimo ir kai kurių mikroorganizmų rezistentiškumo pokyčių analizė." Master's thesis, Lithuanian Academic Libraries Network (LABT), 2008. http://vddb.library.lt/obj/LT-eLABa-0001:E.02~2008~D_20080616_100358-21547.

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Santrauka. Didėjantis mikroorganizmų atsparumas antibiotikams yra aktuali visuomenės sveikatos problema. Vienas iš pagrindinių veiksnių, turinčių įtakos atsparumo plitimui, yra antibakterinių vaistų vartojimas. Darbo tikslas. Nustatyti antibiotikų metinio vartojimo pokyčius bei jų galimas sąsajas su mikroorganizmų rezistentiškumo pokyčiais. Metodas. Tretinio lygio ligoninėje atlikta mikroorganizmų atsparumo ir antibiotikų suvartojimo epidemiologinė analizė. Surinkti duomenys apie antibiotikų suvartojimą 2004- 2007 metais tretinio lygio ligoninėje. Vaistų suvartojimas išreikštas DDD skaičiumi, tenkančiu 100 lovadienių. Ištirtas antibiotikų suvartojimo kitimas 2004- 2007 metais. Panagrinėtas chirurginio profilio skyrių antibiotikų suvartojimas ir jo galimos sąsajos su atliekamų operacijų skaičiumi. Nustatytas kelių dažniausiai vartojamų panašaus veikimo spektro antibiotikų suvartojimas ir jo kitimas 2004–2007 metais tretinio lygio ligoninėje. Nustatytas dviejų svarbių mikroorganizmų (Escherichia coli ir Klebsiella pneumoniae) atsparumo kitimas 2004–2007 metais tretinio lygio ligoninėje bei sąsajos tarp panašaus spektro antibiotikų suvartojimo ir šių mikroorganizmų atsparumo kitimo. Duomenys apdoroti aprašomąja ir lyginamąja statistika (Mann–Whithey testas neparametriniams kriterijams bei Spirmano koreliacija). Rezultatai. 2004 – 2007 metais tretinio lygio ligoninėje statistiškai patikimai didėjo šių antibiotikų suvartojimas: piperacilino–tazobaktamo (877,50 proc.)... [toliau žr. visą tekstą]
Summary. Antimicrobial resistance is a serious public health problem worldwide. Irrational use of antibiotics is one of the reasons of increasing resistance to these preparations. The main goal of this study was to evaluate the variation of antibiotics consumption and relation between antibiotics consumption and microorganism resistance. Method. This analysis was performed in one of Lithuanian tertiary hospitals. The DDD analysis was performed to express consumption per every 100 OBD for single units in clinical departments. Average mean of DDD/100 OBD was estimated for 2004- 2007 years and mean values compared among all four years. The relation between the number of surgical operations and antibiotics consumption in surgery departments was analysed. E.coli and K.pneumoniae resistance for the four financial years (2004- 2007) was determined. Moreover the relation between microorganism resistance and variation of antibiotics consumption was determined. Data were analysed by descriptive and comparative statistics (by Mann–Whithey test for non-parametric criteria and Spirman correlation). Results. Comparing the DDD/100 OBD data year-on-year revealed the statistically significant increase of piperacillin and tazobactam (877.50%), metronidazole (114.00%), cefuroxime (77.31%), meroponem (47.55%), cefoperazone and sulbactam (173.11%) use. The increased usage of these antibiotics was determined in surgery department too. However the increased number of surgical operations can’t be... [to full text]

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Johnson, Rabia. "Understanding the mechanisms of drug resistance in enhancing rapid molecular detection of drug resistance in Mycobacterium tuberculosis." Thesis, Link to the online version, 2007. http://hdl.handle.net/10019.1/1265.

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Joseph, Renu. "Evolution of multiple antimicrobial drug resistance conservation of genes encoding streptomycin, sulfonamide and tetracycline resistance among Escherichia coli with increasing multi-drug resistance /." Online access for everyone, 2007. http://www.dissertations.wsu.edu/Thesis/Fall2007/R_Joseph_111707.pdf.

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Books on the topic "Drug resistance in microorgani"

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C, Crabbe M. James, ed. Bacteria and anti-bacterical agents. Oxford: Spektrum, 1996.

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2

Thompson, Kimberly M. Overkill: How our nation's abuse of antibiotics and other germ killers is hurting your health and what you can do about it. Emmaus, Pa: Rodale, 2002.

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Drug resistance. Tunbridge Wells: Ticktock, 2010.

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Drug resistance. Mankato, MN: New Forest Press, 2010.

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Hait, William N., ed. Drug Resistance. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4613-1267-3.

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Meszaros, Agoston. Multiple drug resistance. New York: Nova Science Publishers, 2010.

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Teicher, Beverly A., ed. Cancer Drug Resistance. Totowa, NJ: Humana Press, 2006. http://dx.doi.org/10.1007/978-1-59745-035-5.

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Goldstein, Lori J., and Robert F. Ozols, eds. Anticancer Drug Resistance. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4615-2632-2.

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Mayers, Douglas L., Jack D. Sobel, Marc Ouellette, Keith S. Kaye, and Dror Marchaim, eds. Antimicrobial Drug Resistance. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-47266-9.

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Mayers, Douglas L., ed. Antimicrobial Drug Resistance. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-595-8.

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Book chapters on the topic "Drug resistance in microorgani"

1

Weber, Georg F. "Drug Resistance." In Molecular Therapies of Cancer, 407–21. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-13278-5_16.

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Tew, Kenneth D. "Drug Resistance." In Basic Science of Cancer, 187–215. London: Current Medicine Group, 2000. http://dx.doi.org/10.1007/978-1-4684-8437-3_10.

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Tomasetti, Cristian. "Drug Resistance." In A Systems Biology Approach to Blood, 303–16. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-2095-2_15.

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Tu, Shi-Ming. "Drug Resistance." In Cancer Treatment and Research, 161–75. Boston, MA: Springer US, 2010. http://dx.doi.org/10.1007/978-1-4419-5968-3_15.

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Saez, S. "Drug Resistance." In Endocrine Therapy of Breast Cancer III, 17–25. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-74504-1_3.

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Wang, Bo. "Drug Resistance." In Encyclopedia of Cancer, 1–4. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-27841-9_1739-7.

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Wang, Bo. "Drug Resistance." In Encyclopedia of Cancer, 1431–34. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-662-46875-3_1739.

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Ford, James M., Jin-Ming Yang, and William N. Hait. "P-Glycoprotein-Mediated Multidrug Resistance: Experimental and Clinical Strategies for its Reversal." In Drug Resistance, 3–38. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4613-1267-3_1.

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Rubin, Eric H., Tsai-Kun Li, Pu Duann, and Leroy F. Liu. "Cellular Resistance to Topoisomerase Poisons." In Drug Resistance, 243–60. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4613-1267-3_10.

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Clarke, Robert, Todd Skaar, Fabio Leonessa, Brenda Brankin, Mattie James, Nils Brünner, and Marc E. Lippman. "Acquisition of an Antiestrogen-Resistant Phenotype in Breast Cancer: Role of Cellular and Molecular Mechanisms." In Drug Resistance, 263–83. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4613-1267-3_11.

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Conference papers on the topic "Drug resistance in microorgani"

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WANG, HONGZHI, XIAOFENG PANG, YIMING WANG, and AIHUA WANG. "TEST OF DRUG RESISTANCE ON BACTERIA WITH IMPEDANCE MICROORGANISM SENSOR." In Proceedings of the 6th International Conference on Photonics and Imaging in Biology and Medicine (PIBM 2007). WORLD SCIENTIFIC, 2008. http://dx.doi.org/10.1142/9789812832344_0060.

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Ayati, Marzieh, Golnaz Taheri, Shahriar Arab, Limsoon Wong, and Changiz Eslahchi. "Overcoming drug resistance by co-targeting." In 2010 IEEE International Conference on Bioinformatics and Biomedicine (BIBM). IEEE, 2010. http://dx.doi.org/10.1109/bibm.2010.5706562.

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Casagrande, Anne-Sophie, Florence Mahe, Vin Kotraiah, Matt Pando, and Laurent Desire. "Abstract 4860: Identification of novel epitopes, drug resistance markers and drug resistance mechanism using alternative splicing studies." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-4860.

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Kai, Masaaki, and Qinchang Zhu. "Convenient drug-resistance testing of HIV mutants." In 1st International Electronic Conference on Medicinal Chemistry. Basel, Switzerland: MDPI, 2015. http://dx.doi.org/10.3390/ecmc-1-a030.

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Alkhovik, Olga, Tatiana Petrenko, and Ivan Meshkov. "Drug resistance of Nontuberculous mycobacteria in Siberia." In ERS International Congress 2019 abstracts. European Respiratory Society, 2019. http://dx.doi.org/10.1183/13993003.congress-2019.pa3636.

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Xiaxia Yu, Robert W. Harrison, and Irene T. Weber. "HIV drug resistance prediction using multiple regression." In 2013 IEEE 3rd International Conference on Computational Advances in Bio and Medical Sciences (ICCABS). IEEE, 2013. http://dx.doi.org/10.1109/iccabs.2013.6629203.

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Sawyers, Charles L. "Abstract PL04-01: Overcoming cancer drug resistance." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-pl04-01.

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Faedo, Ivan, Silvia Martorano Raimundo, Ezio Venturino, Theodore E. Simos, George Psihoyios, and Ch Tsitouras. "A Mathematical Model for HIV Drug-Resistance." In ICNAAM 2010: International Conference of Numerical Analysis and Applied Mathematics 2010. AIP, 2010. http://dx.doi.org/10.1063/1.3498583.

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Javed, Hasnain, and Nazia Jamil. "Genotypes and drug resistance patterns of multi-drug-resistantmycobacterium tuberculosisstrains in Pakistan." In Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.pa2687.

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Li, Hong, Yi-Fei Zhu, Shi-Ying Zheng, and Dong Jiang. "Relationship between methylation status of multi-drug resistance protein (MRP) and multi-drug resistance in lung cancer cell lines." In 2009 International Conference on Future BioMedical Information Engineering (FBIE). IEEE, 2009. http://dx.doi.org/10.1109/fbie.2009.5405779.

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Reports on the topic "Drug resistance in microorgani"

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DeClerck, Yves A. Environment-Mediated Drug Resistance in Neuroblastoma. Fort Belvoir, VA: Defense Technical Information Center, October 2013. http://dx.doi.org/10.21236/ada591172.

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DeClerck, Yves A. Environment-Mediated Drug Resistance in Neuroblastoma. Fort Belvoir, VA: Defense Technical Information Center, October 2014. http://dx.doi.org/10.21236/ada616252.

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Perelson, A. S., B. Goldstein, and B. T. Korber. Emerging pathogens: Dynamics, mutation and drug resistance. Office of Scientific and Technical Information (OSTI), October 1997. http://dx.doi.org/10.2172/534529.

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Hiscott, John. Oncolytic Virotherapy Targeting Lung Cancer Drug Resistance. Fort Belvoir, VA: Defense Technical Information Center, August 2013. http://dx.doi.org/10.21236/ada589848.

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Shen, Youqing, Maciej Radosz, and William J. Murdoch. Breast Cancer-Targeted Nuclear Drug Delivery Overcoming Drug Resistance for Breast Cancer Chemotherapy. Fort Belvoir, VA: Defense Technical Information Center, September 2011. http://dx.doi.org/10.21236/ada559246.

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Kennedy, Katherine A. Physiological Stree-Induced Drug Resistance and Its Reversal. Fort Belvoir, VA: Defense Technical Information Center, July 2001. http://dx.doi.org/10.21236/ada398214.

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Kennedy, Katherine. Physiological Stress-Induced Drug Resistance and Its Reversal. Fort Belvoir, VA: Defense Technical Information Center, July 2000. http://dx.doi.org/10.21236/ada383040.

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Kennedy, Katherine A. Physiological Stress-Induced Drug Resistance and Its Reversal. Fort Belvoir, VA: Defense Technical Information Center, July 2002. http://dx.doi.org/10.21236/ada408700.

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Kennedy, Katherine. Physiological Stress-Induced Drug Resistance and its Reversal. Fort Belvoir, VA: Defense Technical Information Center, July 2004. http://dx.doi.org/10.21236/ada474449.

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Shannon, Kevin. Drug Response and Resistance in Advanced NF1-Associated Cancers. Fort Belvoir, VA: Defense Technical Information Center, April 2013. http://dx.doi.org/10.21236/ada581891.

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