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Artigos de revistas sobre o tema "Drug Resistance"

Autor: Grafiati

Publicado: 4 de junho de 2021

Última modificação: 2 de novembro de 2024

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1

K, Tiwari. "Drug Resistance: Challenges and Updates". Journal of Natural & Ayurvedic Medicine 3, n.º 3 (15 de julho de 2019): 1–2. http://dx.doi.org/10.23880/jonam-16000196.

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Use of antibiotics increased dramatically in last two decades. To cure most of the diseases broad spectrum antibiotics given. Human society and healthcare is going in wrong direction. One way the pharmaceutical companies are making huge money from it. The other way around is the overuse of these antibiotics, by patients knowing or unknowingly, not only making pathogens adapted but also the normal flora organisms becoming pathogens in coming future? Present article highlight the issues and possible solution of the present scenario.

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2

Singh, Amresh Kumar. "Resistance patterns and trends of extensively drug-resistant tuberculosis: 5-year experience". Journal of Microbiology and Infectious Diseases 03, n.º 04 (1 de dezembro de 2013): 169–75. http://dx.doi.org/10.5799/ahinjs.02.2013.04.0103.

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3

Dyary, Hiewa Othman. "Veterinary Anthelmintics and Anthelmintic Drug Resistance". Journal of Zankoy Sulaimani - Part A 18, n.º 1 (12 de novembro de 2015): 191–206. http://dx.doi.org/10.17656/jzs.10463.

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4

Çelik, Cem. "Increasing antimicrobial resistance in nosocomial pathogens; multidrug-resistant extensively drug-resistant and pandrug-resistant Acinetobacter baumannii". Journal of Microbiology and Infectious Diseases 4, n.º 1 (1 de março de 2014): 7–12. http://dx.doi.org/10.5799/ahinjs.02.2014.01.0116.

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5

Giaccone, Giuseppe, e Herbert M. Pinedo. "Drug Resistance". Oncologist 1, n.º 1-2 (fevereiro de 1996): 82–87. http://dx.doi.org/10.1634/theoncologist.1-1-82.

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6

Hochhauser, D., e A. L. Harris. "Drug resistance". British Medical Bulletin 47, n.º 1 (1991): 178–96. http://dx.doi.org/10.1093/oxfordjournals.bmb.a072454.

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7

Prichard, R. K. "Drug resistance". International Journal for Parasitology 29, n.º 1 (janeiro de 1999): 137–38. http://dx.doi.org/10.1016/s0020-7519(98)00191-x.

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8

Texidó, Gemma, e Jürgen Moll. "Drug resistance". Drug Discovery Today: Technologies 11 (março de 2014): 1–3. http://dx.doi.org/10.1016/j.ddtec.2014.03.013.

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9

Köser, Claudio U., Babak Javid, Kathleen Liddell, Matthew J. Ellington, Silke Feuerriegel, Stefan Niemann, Nicholas M. Brown et al. "Drug-resistance mechanisms and tuberculosis drugs". Lancet 385, n.º 9965 (janeiro de 2015): 305–7. http://dx.doi.org/10.1016/s0140-6736(14)62450-8.

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10

Coen, Donald M., e Richard J. Whitley. "Antiviral drugs and antiviral drug resistance". Current Opinion in Virology 1, n.º 6 (dezembro de 2011): 545–47. http://dx.doi.org/10.1016/j.coviro.2011.10.024.

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11

Hall, Andrew G., e Julie Irving. "New drugs, new drug resistance mechanisms". Expert Review of Anticancer Therapy 2, n.º 3 (junho de 2002): 239–340. http://dx.doi.org/10.1586/14737140.2.3.239.

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12

Kumar, Saurabh, e Richa Prasad Mahato. "DRUG RESISTANCE AND RESISTANCE REVERSAL STRATEGIES IN MALARIA PARASITE". Journal of microbiology, biotechnology and food sciences 13, n.º 5 (5 de fevereiro de 2024): e10384. http://dx.doi.org/10.55251/jmbfs.10384.

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The public health care system is currently facing a major problem with malaria. Globally, malarial deaths have decreased by an estimated 40% in the past two decades because of the clinically effective drugs (artemisinin-based combination therapies) against Plasmodium falciparum. In recent years, P falciparum develop resistance against all antimalarial drugs and then becomes developed multidrug resistance that a major challenge. Even though drug discovery programs have made substantial progress in the past decade, the potential for new drugs/combinations to improve the effectiveness of current malaria control strategies. Beyond, we have compiled a comprehensive review of clinically approved anti-malarial drugs with resistance mechanisms and a novel drug-resistance reversal approach in one place to meet this demand. The review aimed to provide detailed information on drug resistance, its regulatory molecular mechanisms responsible for resistance, and the novel available treatment of malaria. In this review, the article will help in developing effective interventions, potential approaches, and strategies to handle antimalarial resistance. This will prevent life-threatening infections.

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13

Yusuf, Yenni. "ANTI-MALARIAL DRUG RESISTANCE". Majalah Kedokteran Andalas 37, n.º 1 (3 de maio de 2015): 64. http://dx.doi.org/10.22338/mka.v37.i1.p64-69.2014.

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AbstrakTujuan studi ini adalah untuk menjelaskan mekanisme resistensi parasit malaria danusaha-usaha yang dapat dilakukan untuk menghadapi munculnya strain parasit yangresisten terhadap artemisinin. Metode yang digunakan adalah studi kepustakaan. ResistensiP.falciparum terhadap obat-obat anti malaria disebabkan oleh perubahan spontan yangterjadi pada beberapa gen seperti P.falciparum multi drug resistance1 (Pfmdr1), P.falciparumchloroquine transporter (Pfcrt), P.falciparum dihydropteroate synthase (Pfdhps), P.falciparumdihydrofolate reductase (Pfdhfr), and P.falciparum multidrug resistance-associated proteins(Pfmrp). Penyebaran resistensi tersebut dipengaruhi oleh tingkat transmisi di sebuah wilayah.WHO telah menjalankan usaha untuk menanggulangi penyebaran resistensi tersebut misalnyadengan merekomendasikan penghentian monoterapi artemisinin, dan pemberian anti malariasetelah konfirmasi laboratorium. Selain itu, perlu adanya penggunaan obat kombinasi, produksirejimen dosis tetap, dan pengembangan obat anti malaria baru. Kesimpulan dari hasil studiini ialah munculnya malaria resisten terhadap artemisinin akan menghambat usaha eradikasimalaria karena itu diperlukan usaha-usaha untuk menanggulanginya.AbstractThe objective of this study was to describe the development of anti-malarial drug resistanceof the parasites and the efforts taken to contain the emergence of artemisinin resistant malaria.This was a literature study. The development of resistance to anti-malarial drugs are due tospontaneous changes in certain genes such as of P.falciparum multi drug resistance1 (Pfmdr1),P.falciparum chloroquine resistance transporter (Pfcrt), P.falciparum dihydropteroate synthase(Pfdhps), P.falciparum dihydrofolate reductase (Pfdhfr), and P.falciparum multidrug resistanceassociatedproteins (Pfmrp). The spread of the resistance depends on the transmission ratewithin each area. WHO has established a global plan to contain the spread of this resistance,such as recommendation to withdraw artemisinin-based monotherapies and administrationof treatment after laboratory confirmation. In addition, administration of anti-malarial drugcombination, production of fixed dose regimen and development of new drugs are necessary.The Conclusion is emergence of artemisinin resistant malaria will threaten malaria eradicationthus some efforts are necessarily needed to contain it.Afiliasi penulis: Bagian Parasitologi Fakultas Kedokteran Universitas Hasanudin

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14

Nyce, J., S. Leonard, D. Canupp, S. Schulz e S. Wong. "Epigenetic mechanisms of drug resistance: drug-induced DNA hypermethylation and drug resistance." Proceedings of the National Academy of Sciences 90, n.º 7 (1 de abril de 1993): 2960–64. http://dx.doi.org/10.1073/pnas.90.7.2960.

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15

Hossain, Chowdhury Mobaswar, Lisa Kathleen Ryan, Meeta Gera, Sabyasachi Choudhuri, Nazmun Lyle, Kazi Asraf Ali e Gill Diamond. "Antifungals and Drug Resistance". Encyclopedia 2, n.º 4 (10 de outubro de 2022): 1722–37. http://dx.doi.org/10.3390/encyclopedia2040118.

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Antifungal drugs prevent topical or invasive fungal infections (mycoses) either by stopping growth of fungi (termed fungistatic) or by killing the fungal cells (termed fungicidal). Antibiotics also prevent bacterial infections through either bacteriostatic or bactericidal mechanisms. These microorganisms successfully develop resistance against conventional drugs that are designed to kill or stop them from multiplying. When a fungus no longer responds to antifungal drug treatments and continues to grow, this is known as antifungal drug resistance. Bacteria have an amazing capacity to become resistant to antibiotic action as well, and the effectiveness of the scarce antifungal arsenal is jeopardised by this antibiotic resistance, which poses a severe threat to public health.

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16

Perfect, John R., e Gary M. Cox. "Drug resistance in Cryptococcus neoformans". Drug Resistance Updates 2, n.º 4 (agosto de 1999): 259–69. http://dx.doi.org/10.1054/drup.1999.0090.

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17

Kennedy, David A., e Andrew F. Read. "Why does drug resistance readily evolve but vaccine resistance does not?" Proceedings of the Royal Society B: Biological Sciences 284, n.º 1851 (29 de março de 2017): 20162562. http://dx.doi.org/10.1098/rspb.2016.2562.

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Why is drug resistance common and vaccine resistance rare? Drugs and vaccines both impose substantial pressure on pathogen populations to evolve resistance and indeed, drug resistance typically emerges soon after the introduction of a drug. But vaccine resistance has only rarely emerged. Using well-established principles of population genetics and evolutionary ecology, we argue that two key differences between vaccines and drugs explain why vaccines have so far proved more robust against evolution than drugs. First, vaccines tend to work prophylactically while drugs tend to work therapeutically. Second, vaccines tend to induce immune responses against multiple targets on a pathogen while drugs tend to target very few. Consequently, pathogen populations generate less variation for vaccine resistance than they do for drug resistance, and selection has fewer opportunities to act on that variation. When vaccine resistance has evolved, these generalities have been violated. With careful forethought, it may be possible to identify vaccines at risk of failure even before they are introduced.

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18

Croft, Simon L., Shyam Sundar e Alan H. Fairlamb. "Drug Resistance in Leishmaniasis". Clinical Microbiology Reviews 19, n.º 1 (janeiro de 2006): 111–26. http://dx.doi.org/10.1128/cmr.19.1.111-126.2006.

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SUMMARY Leishmaniasis is a complex disease, with visceral and cutaneous manifestations, and is caused by over 15 different species of the protozoan parasite genus Leishmania. There are significant differences in the sensitivity of these species both to the standard drugs, for example, pentavalent antimonials and miltefosine, and those on clinical trial, for example, paromomycin. Over 60% of patients with visceral leishmaniasis in Bihar State, India, do not respond to treatment with pentavalent antimonials. This is now considered to be due to acquired resistance. Although this class of drugs has been used for over 60 years for leishmaniasis treatment, it is only in the past 2 years that the mechanisms of action and resistance have been identified, related to drug metabolism, thiol metabolism, and drug efflux. With the introduction of new therapies, including miltefosine in 2002 and paromomycin in 2005-2006, it is essential that there be a strategy to prevent the emergence of resistance to new drugs; combination therapy, monitoring of therapy, and improved diagnostics could play an essential role in this strategy.

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19

de Koning, Harry P. "Drug resistance in protozoan parasites". Emerging Topics in Life Sciences 1, n.º 6 (22 de dezembro de 2017): 627–32. http://dx.doi.org/10.1042/etls20170113.

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As with all other anti-infectives (antibiotics, anti-viral drugs, and anthelminthics), the limited arsenal of anti-protozoal drugs is being depleted by a combination of two factors: increasing drug resistance and the failure to replace old and often shamefully inadequate drugs, including those compromised by (cross)-resistance, through the development of new anti-parasitics. Both factors are equally to blame: a leaking bathtub may have plenty of water if the tap is left open; if not, it will soon be empty. Here, I will reflect on the factors that contribute to the drug resistance emergency that is unfolding around us, specifically resistance in protozoan parasites.

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20

Kurt Yilmaz, Nese, e Celia A. Schiffer. "Introduction: Drug Resistance". Chemical Reviews 121, n.º 6 (24 de março de 2021): 3235–37. http://dx.doi.org/10.1021/acs.chemrev.1c00118.

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21

Emery, VC. "Cytomegalovirus Drug Resistance". Antiviral Therapy 3, n.º 4 (maio de 1998): 239–42. http://dx.doi.org/10.1177/135965359800300403.

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Clinical resistance of cytomegalovirus (CMV) against the currently licensed antiviral drugs is becoming an increasingly recognized problem. This review focuses on the molecular basis of resistance and describes mutations in the UL54 DNA polymerase leading to resistance against cidofovir, foscarnet and ganciclovir. The review highlights two important developments in our appreciation of resistance. Firstly, the use of more rapid molecular based assays to detect genotypic resistance and secondly, the relationship between resistance profiles in multiple organ systems of the same host. Finally, the changing face of CMV disease in the era of highly active antiviral chemotherapy is considered with respect to its impact on the frequency of CMV resistance in the clinic.

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22

Clavel, François, e Allan J. Hance. "HIV Drug Resistance". New England Journal of Medicine 350, n.º 10 (4 de março de 2004): 1023–35. http://dx.doi.org/10.1056/nejmra025195.

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23

Richman, D. D. "HIV Drug Resistance". Annual Review of Pharmacology and Toxicology 33, n.º 1 (abril de 1993): 149–64. http://dx.doi.org/10.1146/annurev.pa.33.040193.001053.

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24

Davies, Peter, e Damian Cullen. "Antituberculosis drug resistance". Clinical Medicine 9, n.º 1 (1 de fevereiro de 2009): 91.1–91. http://dx.doi.org/10.7861/clinmedicine.9-1-91.

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25

Perrin, Luc. "Drug resistance mutations". AIDS 18, n.º 8 (maio de 2004): 1201–2. http://dx.doi.org/10.1097/00002030-200405210-00014.

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26

White, Nicholas J. "Antimalarial drug resistance". Journal of Clinical Investigation 113, n.º 8 (15 de abril de 2004): 1084–92. http://dx.doi.org/10.1172/jci21682.

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27

Tesio, Melania. "Starving Drug Resistance". HemaSphere 4, n.º 6 (10 de novembro de 2020): e495. http://dx.doi.org/10.1097/hs9.0000000000000495.

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28

Pizzorno, Andrés, Yacine Abed e Guy Boivin. "Influenza Drug Resistance". Seminars in Respiratory and Critical Care Medicine 32, n.º 04 (agosto de 2011): 409–22. http://dx.doi.org/10.1055/s-0031-1283281.

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29

COEN, DONALD M. "Antiviral Drug Resistance". Annals of the New York Academy of Sciences 616, n.º 1 AIDS (dezembro de 1990): 224–36. http://dx.doi.org/10.1111/j.1749-6632.1990.tb17843.x.

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30

Weitzman, Jonathan B. "Cancer drug resistance". Genome Biology 2 (2001): spotlight—20010626–01. http://dx.doi.org/10.1186/gb-spotlight-20010626-01.

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31

Flintoff, Wayne F. "Acquired drug resistance". Genome 31, n.º 1 (1 de janeiro de 1989): 447. http://dx.doi.org/10.1139/g89-073.

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32

Gold, Howard S., e Robert C. Moellering. "Antimicrobial-Drug Resistance". New England Journal of Medicine 335, n.º 19 (7 de novembro de 1996): 1445–53. http://dx.doi.org/10.1056/nejm199611073351907.

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33

Phelps, Charles E. "Bug/Drug Resistance". Medical Care 27, n.º 2 (fevereiro de 1989): 194–203. http://dx.doi.org/10.1097/00005650-198902000-00009.

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34

Robertson, John D. "CANCER DRUG RESISTANCE". Shock 26, n.º 6 (dezembro de 2006): 638. http://dx.doi.org/10.1097/01.shk.0000248599.09507.90.

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35

RICHMAN, DOUGLAS D. "HIV Drug Resistance". AIDS Research and Human Retroviruses 8, n.º 6 (junho de 1992): 1065–71. http://dx.doi.org/10.1089/aid.1992.8.1065.

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36

Schmit, Jean-Claude. "HIV drug resistance". HIV Clinical Trials 3, n.º 3 (maio de 2002): 225–26. http://dx.doi.org/10.1310/kmkn-ke48-2gwu-g0he.

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37

Richman, Douglas D. "Viral drug resistance". Current Opinion in Infectious Diseases 3, n.º 6 (dezembro de 1990): 819–23. http://dx.doi.org/10.1097/00001432-199012000-00014.

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38

Loeffler, Juergen, e David A. Stevens. "Antifungal Drug Resistance". Clinical Infectious Diseases 36, Supplement_1 (15 de janeiro de 2003): S31—S41. http://dx.doi.org/10.1086/344658.

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39

Richman, Douglas D. "Antiviral drug resistance". Antiviral Research 71, n.º 2-3 (setembro de 2006): 117–21. http://dx.doi.org/10.1016/j.antiviral.2006.03.004.

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40

Calmy, Alexandra, Fernando Pascual e Nathan Ford. "HIV Drug Resistance". New England Journal of Medicine 350, n.º 26 (24 de junho de 2004): 2720–21. http://dx.doi.org/10.1056/nejm200406243502621.

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41

Pillay, D., e A. M. Geddes. "Antiviral drug resistance". BMJ 313, n.º 7056 (31 de agosto de 1996): 503–4. http://dx.doi.org/10.1136/bmj.313.7056.503.

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42

Richman, Douglas D. "Antiretroviral drug resistance". AIDS 5, Supplement (janeiro de 1991): 189. http://dx.doi.org/10.1097/00002030-199101001-00027.

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43

Richman, Douglas D. "HIV DRUG RESISTANCE". AIDS 8, Supplement 4 (novembro de 1994): S3. http://dx.doi.org/10.1097/00002030-199411004-00010.

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44

STEVENSON, AUDREY M. "Emerging Drug Resistance". MCN, The American Journal of Maternal/Child Nursing 23, n.º 4 (julho de 1998): 216. http://dx.doi.org/10.1097/00005721-199807000-00010.

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45

Pillay, D., e M. Zambon. "Antiviral drug resistance". BMJ 317, n.º 7159 (5 de setembro de 1998): 660–62. http://dx.doi.org/10.1136/bmj.317.7159.660.

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46

Field, Hugh J., e Siân E. Goldthorpe. "Antiviral drug resistance". Trends in Pharmacological Sciences 10, n.º 8 (agosto de 1989): 333–37. http://dx.doi.org/10.1016/0165-6147(89)90069-2.

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47

Dannenberg, Jan-Hermen, e Anton Berns. "Drugging Drug Resistance". Cell 141, n.º 1 (abril de 2010): 18–20. http://dx.doi.org/10.1016/j.cell.2010.03.020.

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48

Hampton, Tracy. "Cancer Drug Resistance". JAMA 309, n.º 1 (2 de janeiro de 2013): 20. http://dx.doi.org/10.1001/jama.2012.173440.

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49

McCloskey, William W. "Microbial Drug Resistance". JAMA: The Journal of the American Medical Association 278, n.º 6 (13 de agosto de 1997): 523. http://dx.doi.org/10.1001/jama.1997.03550060099047.

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50

Hampton, Tracy. "Melanoma Drug Resistance". JAMA 296, n.º 4 (26 de julho de 2006): 384. http://dx.doi.org/10.1001/jama.296.4.384-b.

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