Author:
- INTRODUCTION
- MATERIALS AND METHODS
- RESULTS
- Clinical and parasitologic resistance to S/P in Hag Yousif (Sudan), Kibaha (Tanzania), Matola (Mozambique) and Magoda (Tanzania).
- Frequency of mutations in dhfr and dhps in relation to in vivo outcome of S/P treatment.
- Prevalence of combinations of mutations in dhfr.
- Prevalence of combinations of mutations in dhfr and c437 of dhps.
- DISCUSSION
ProCite
RefWorks
Reference Manager
BibTeX
Zotero
EndNote
-
1
Cowman A, Morry MJ, Biggs BA, Cross GAM, Foote SJ, 1988. Amino acid changes linked to pyrimethamine resistance in the dihydrofolate reductase-thymidylate synthase gene of Plasmodium falciparum.Proc Natl Acad Sci USA 85 :9109–9113.
-
2
Snewin VA, England SM, Sims PF, Hyde JE, 1989. Characterisation of the dihydrofolate reductase-thymidylate synthetase gene from human malaria parasites highly resistant to pyrimethamine. Gene 76 :41–52.
-
3
Hyde JE, 1990. The dihydrofolate reductase-thymidylate synthetase gene in the drug resistance of malaria parasites. Pharmacol Ther 48 :45–59.
-
4
Sirawaraporn W, Sathitkul T, Sirawaraporn R, Yuthavong Y, Santi DV, 1997. Antifolate-resistant mutants of Plasmodium falciparum dihydrofolate reductase. Proc Natl Acad Sci USA 94 :1124–1129.
-
5
Brooks R, Wang P, Read M, Watkins MW, Sims PFG, Hyde JE, 1994. Sequence variation of the hydroxymethyldihydropterin pyrophosphokinase: dihydropteroate synthase gene lines of the human malaria parasite, Plasmodium falciparum, with differing resistance to sulfadoxine. J Biochem 224 :397–405.
-
6
Triglia T, Cowman A, 1994. Primary structure and expression of the dihydropteroate synthetase gene of Plasmodium falciparum.Proc Natl Acad Sci USA 91 :7149–7153.
-
7
Wang P, Read M, Sims PFG, Hyde JE, 1997. Sulfadoxine resistance in the human malaria parasite Plasmodium falciparum is determined by mutations in dihydropteroate synthetase and an additional factor associated with folate utilization. Mol Microbiol 23 :979–986.
-
8
Plowe CV, Djimde A, Bouare M, Doumbo O, Wellems TE, 1995. Pyrimethamine and proguanil resistance-conferring mutations in Plasmodium falciparum dihydrofolate reductase: polymerase chain reaction methods for surveillance in Africa. Am J Trop Med Hyg 52 :565–568.
-
9
Omar SA, Adagu IS, Warhurst DC, 2001. Can pretreatment screening for dhps and dhfr point mutations in Plasmodium falciparum infections be used to predict sulfadoxine-pyrimethamine treatment failure? Trans R Soc Trop Med Hyg 95 :315–319.
-
10
Basco LK, Tahar R, Keundjian A, Ringwald P, 2000. Sequence variations in the genes encoding dihydropteroate synthase and dihydrofolate reductase and clinical response to sulfadoxine-pyrimethamine in patients with acute uncomplicated falciparum malaria. J Infect Dis 182 :624–628.
-
11
Wang P, Lee C-S, Bayoumi R, Djimde A, Doumbo O, Swedberg G, Dao LD, Mshinda H, Tanner M, Watkins MW, Sims PFG, Hyde JE, 1997. Resistance to antifolates in Plasmodium falciparum monitored by sequence analysis of dihydropteroate synthetase and dihydrofolate reductase alleles in a large number of field samples of diverse origins. Mol Biochem Parasitol 89 :161–177.
-
12
Plowe CV, Cortese JF, Djimde A, Nwanyanwu OC, Watkins WM, Winstanley PA, Estrada-Franco JG, Mollinedo RE, Avila JC, Cespedes JL, Carter D, Doumbo OK, 1997. Mutations in Plasmodium falciparum dihydrofolate reductase and dihydropteroate synthase and epidemiologic patterns of pyrimethamine-sulfadoxine use and resistance. J Infect Dis 176 :1590–1596.
-
13
Kublin JG, Dzinjalamala FK, Kamwendo DD, Malkin EM, Cortese JF, Martino LM, Mukadam RA, Rogerson SJ, Lescano AG, Molyneux ME, Winstanley PA, Chimpeni P, Taylor TE, Plowe CV, 2002. Molecular markers for failure of sulfadoxine-pyrimethamine and chlorproguanil-dapsone treatment of Plasmodium falciparum malaria. J Infect Dis 185 :380–388.
-
14
Rallon NI, Osorio LE, Giraldo LE, 1999. Lack of an association between the ASN-108 mutation in the dihydrofolate reductase gene and in vivo resistance to sulfadoxine/pyrimethamine in Plasmodium falciparum.Am J Trop Med Hyg 61 :245–248.
-
15
Kublin JG, Witzig RS, Shankar AH, Zurita JQ, Gilman RH, Guarda JA, Cortese JF, Plowe CV, 1998. Molecular assays for surveillance of antifolate-resistant malaria. Lancet 351 :1629–1630.
-
16
Khalil I, Alifrangis M, Ronn AM, Gabar HA, Jelinek T, Satti GM, Bygbjerg IC, 2002. Pyrimethamine/sulfadoxine combination in the treatment of uncomplicated falciparum malaria: relation between dihydropteroate synthase/dihydrofolate reductase genotypes, sulfadoxine plasma levels, and treatment outcome. Am J Trop Med Hyg 67 :225–229.
-
17
Nzila AM, Nduati E, Mberu EK, Hopkins SC, Monks SA, Winstanley PA, Watkins WM, 2000. Molecular evidence of greater selective pressure for drug resistance exerted by the long-acting antifolate pyrimethamine/sulfadoxine compared with the shorter-acting chlorproguanil/dapsone on Kenyan Plasmodium falciparum.J Infect Dis 181 :2023–2028.
-
18
Nagesha HS, Din S, Casey GJ, Susanti AI, Fryauff DJ, Reeder JC, Cowman AF, 2001. Mutations in the pfmdr1, dhfr and dhps genes of Plasmodium falciparum are associated with in-vivo drug resistance in West Papua, Indonesia. Trans R Soc Trop Med Hyg 95 :43–49.
-
19
WHO, 1973. Chemotherapy of malaria and resistance to antimalarial drugs. World Health Organ Tech Rep Ser 529.
-
20
WHO, 1996. Assessment of Therapeutic Efficacy of Antimalarial Drugs - For Uncomplicated Falciparum Malaria in Areas with Intense Transmission. Geneva: World Health Organization, WHO/MAL/96.1077.
-
21
Tarimo DS, Minjas JN, Bygbjerg IC, 2002. Sulfadoxine-pyrimethamine monotherapy in Tanzanian children gives rapid parasite clearance but slow fever clearance that is improved by chloroquine in combination therapy. Trop Med Int Health 7 :592–598.
-
22
Thompson R, Begtrup K, Cuamba N, Dgedge M, Mendis C, Gamage-Mendis A, Enosse SM, Barreto J, Sinden RE, Hogh B, 1997. The Matola malaria project: a temporal and spatial study of malaria transmission and disease in a suburban area of Maputo, Mozambique. Am J Trop Med Hyg 57 :550–559.
-
23
Lemnge MM, Msangeni HA, Rønn AM, Salum FM, Jakobsen PH, Mhina J, Akida JA, Bygbjerg IC, 1997. Maloprim malaria prophylaxis in children living in a holoendemic village in north-eastern Tanzania. Trans R Soc Trop Med Hyg 91 :68–73.
-
24
Sambrook J, Fritsch EF, Maniatis T, 1989. Molecular Cloning: A Laboratory Manual. Second edition. Cold Spring Harbor, NY: Cold Spring Harbor Laboratory Press.
-
25
Wooden J, Kyes S, Sibley CH, 1993. PCR and strain identification in Plasmodium falciparum.Parasitol Today 9 :303–305.
-
26
Duraisingh MT, Curtis J, Warhurst DC, 1998. Plasmodium falciparum: detection of polymorphisms in the dihydrofolate reductase and dihydropteroate synthetase genes by PCR and restriction digestion. Exp Parasitol 89 :1–8.
-
27
Jelinek T, Rønn AM, Lemnge MM, Curtis J, Mhina J, Duraisingh MT, Bygbjerg IC, Warhurst DC, 1998. Polymorphisms in dihydrofolate reductase (DHFR) and dihydropteroate synthetase (DHPS) genes of Plasmodium falciparum and in vivo resistance to sulfadoxine/pyrimethamine in isolates from Tanzania. Trop Med Int Health 3 :605–609.
-
28
Mutabingwa T, Nzila A, Mberu E, Nduati E, Winstanley P, Hills E, Watkins W, 2001. Chlorproguanil-dapsone for treatment of drug-resistant falciparum malaria in Tanzania. Lancet 358 :1218–1223.
-
29
Magesa SM, Mdira KY, Farnert A, Simonsen PE, Bygbjerg IC, Jakobsen PH, 2001. Distinguishing Plasmodium falciparum treatment failures from re-infections by using polymerase chain reaction genotyping in a holoendemic area in northeastern Tanzania. Am J Trop Med Hyg 65 :477–483.
| Past two years | Past Year | Past 30 Days | |
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PREDICTION OF PLASMODIUM FALCIPARUM RESISTANCE TO SULFADOXINE/ PYRIMETHAMINE IN VIVO BY MUTATIONS IN THE DIHYDROFOLATE REDUCTASE AND DIHYDROPTEROATE SYNTHETASE GENES: A COMPARATIVE STUDY BETWEEN SITES OF DIFFERING ENDEMICITY
MICHAEL ALIFRANGIS
MICHAEL ALIFRANGIS
Centre for Medical Parasitology, Institute of Medical Microbiology and Immunology, and Institute of Public Health, University of Copenhagen and Department of Infectious Diseases, Copenhagen University Hospital, Copenhagen, Denmark; National Institute of Health, Ministry of Health, Maputo, Mozambique; Faculty of Medicine, Muhimbili University, Dar es Salaam, Tanzania; National Institute for Medical Research, Amani Research Centre, Amani, Tanzania
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SONJA ENOSSE
SONJA ENOSSE
Centre for Medical Parasitology, Institute of Medical Microbiology and Immunology, and Institute of Public Health, University of Copenhagen and Department of Infectious Diseases, Copenhagen University Hospital, Copenhagen, Denmark; National Institute of Health, Ministry of Health, Maputo, Mozambique; Faculty of Medicine, Muhimbili University, Dar es Salaam, Tanzania; National Institute for Medical Research, Amani Research Centre, Amani, Tanzania
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INSAF F. KHALIL
INSAF F. KHALIL
Centre for Medical Parasitology, Institute of Medical Microbiology and Immunology, and Institute of Public Health, University of Copenhagen and Department of Infectious Diseases, Copenhagen University Hospital, Copenhagen, Denmark; National Institute of Health, Ministry of Health, Maputo, Mozambique; Faculty of Medicine, Muhimbili University, Dar es Salaam, Tanzania; National Institute for Medical Research, Amani Research Centre, Amani, Tanzania
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DONATH S. TARIMO
DONATH S. TARIMO
Centre for Medical Parasitology, Institute of Medical Microbiology and Immunology, and Institute of Public Health, University of Copenhagen and Department of Infectious Diseases, Copenhagen University Hospital, Copenhagen, Denmark; National Institute of Health, Ministry of Health, Maputo, Mozambique; Faculty of Medicine, Muhimbili University, Dar es Salaam, Tanzania; National Institute for Medical Research, Amani Research Centre, Amani, Tanzania
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MARTHA M. LEMNGE
MARTHA M. LEMNGE
Centre for Medical Parasitology, Institute of Medical Microbiology and Immunology, and Institute of Public Health, University of Copenhagen and Department of Infectious Diseases, Copenhagen University Hospital, Copenhagen, Denmark; National Institute of Health, Ministry of Health, Maputo, Mozambique; Faculty of Medicine, Muhimbili University, Dar es Salaam, Tanzania; National Institute for Medical Research, Amani Research Centre, Amani, Tanzania
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RICHARDO THOMPSON
RICHARDO THOMPSON
Centre for Medical Parasitology, Institute of Medical Microbiology and Immunology, and Institute of Public Health, University of Copenhagen and Department of Infectious Diseases, Copenhagen University Hospital, Copenhagen, Denmark; National Institute of Health, Ministry of Health, Maputo, Mozambique; Faculty of Medicine, Muhimbili University, Dar es Salaam, Tanzania; National Institute for Medical Research, Amani Research Centre, Amani, Tanzania
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IB C. BYGBJERG
IB C. BYGBJERG
Centre for Medical Parasitology, Institute of Medical Microbiology and Immunology, and Institute of Public Health, University of Copenhagen and Department of Infectious Diseases, Copenhagen University Hospital, Copenhagen, Denmark; National Institute of Health, Ministry of Health, Maputo, Mozambique; Faculty of Medicine, Muhimbili University, Dar es Salaam, Tanzania; National Institute for Medical Research, Amani Research Centre, Amani, Tanzania
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ANITA M. RØNN
ANITA M. RØNN
Centre for Medical Parasitology, Institute of Medical Microbiology and Immunology, and Institute of Public Health, University of Copenhagen and Department of Infectious Diseases, Copenhagen University Hospital, Copenhagen, Denmark; National Institute of Health, Ministry of Health, Maputo, Mozambique; Faculty of Medicine, Muhimbili University, Dar es Salaam, Tanzania; National Institute for Medical Research, Amani Research Centre, Amani, Tanzania
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Plasmodium falciparum resistance to sulfadoxine/pyrimethamine (S/P) is due to mutations in the dihydrofolate reductase (dhfr) and dihydropteroate synthetase (dhfr) genes. Large-scale screening of the prevalence of these mutations could facilitate the surveillance of the level of S/P resistance in vivo. The prevalence of mutations in dhfr and dhps in relation to S/P efficacy was studied in four sites of differing endemicity in Sudan, Mozambique, and Tanzania. The sites were organized in order of increasing resistance and a significant increase in the prevalence of triple mutations in codons c51, c59, and c108 of dhfr was observed. A similar trend was observed when dhfr genotypes were combined with c437 of dhps. Since the differences in S/P resistance between the sites were minor, but nevertheless revealed major differences in dhfr genotype prevalence, the role of dhfr as a general molecular marker seems debatable. The differences may reflect variation in the duration and magnitude of S/P usage (or other antifolate drugs) between the sites. Thus, triple dhfr mutations may prove suitable only as a general guideline for detecting emerging S/P resistance in areas where S/P has been introduced recently. However, changes in susceptibility within the same area with moderate levels of resistance may be possible by longitudinal surveillance of a subset of dhfr/dhps mutations that has been associated with S/P resistance in vivo in a defined location.
Author Notes
- INTRODUCTION
- MATERIALS AND METHODS
- RESULTS
- Clinical and parasitologic resistance to S/P in Hag Yousif (Sudan), Kibaha (Tanzania), Matola (Mozambique) and Magoda (Tanzania).
- Frequency of mutations in dhfr and dhps in relation to in vivo outcome of S/P treatment.
- Prevalence of combinations of mutations in dhfr.
- Prevalence of combinations of mutations in dhfr and c437 of dhps.
- DISCUSSION
ProCite
RefWorks
Reference Manager
BibTeX
Zotero
EndNote
-
1
Cowman A, Morry MJ, Biggs BA, Cross GAM, Foote SJ, 1988. Amino acid changes linked to pyrimethamine resistance in the dihydrofolate reductase-thymidylate synthase gene of Plasmodium falciparum.Proc Natl Acad Sci USA 85 :9109–9113.
-
2
Snewin VA, England SM, Sims PF, Hyde JE, 1989. Characterisation of the dihydrofolate reductase-thymidylate synthetase gene from human malaria parasites highly resistant to pyrimethamine. Gene 76 :41–52.
-
3
Hyde JE, 1990. The dihydrofolate reductase-thymidylate synthetase gene in the drug resistance of malaria parasites. Pharmacol Ther 48 :45–59.
-
4
Sirawaraporn W, Sathitkul T, Sirawaraporn R, Yuthavong Y, Santi DV, 1997. Antifolate-resistant mutants of Plasmodium falciparum dihydrofolate reductase. Proc Natl Acad Sci USA 94 :1124–1129.
-
5
Brooks R, Wang P, Read M, Watkins MW, Sims PFG, Hyde JE, 1994. Sequence variation of the hydroxymethyldihydropterin pyrophosphokinase: dihydropteroate synthase gene lines of the human malaria parasite, Plasmodium falciparum, with differing resistance to sulfadoxine. J Biochem 224 :397–405.
-
6
Triglia T, Cowman A, 1994. Primary structure and expression of the dihydropteroate synthetase gene of Plasmodium falciparum.Proc Natl Acad Sci USA 91 :7149–7153.
-
7
Wang P, Read M, Sims PFG, Hyde JE, 1997. Sulfadoxine resistance in the human malaria parasite Plasmodium falciparum is determined by mutations in dihydropteroate synthetase and an additional factor associated with folate utilization. Mol Microbiol 23 :979–986.
-
8
Plowe CV, Djimde A, Bouare M, Doumbo O, Wellems TE, 1995. Pyrimethamine and proguanil resistance-conferring mutations in Plasmodium falciparum dihydrofolate reductase: polymerase chain reaction methods for surveillance in Africa. Am J Trop Med Hyg 52 :565–568.
-
9
Omar SA, Adagu IS, Warhurst DC, 2001. Can pretreatment screening for dhps and dhfr point mutations in Plasmodium falciparum infections be used to predict sulfadoxine-pyrimethamine treatment failure? Trans R Soc Trop Med Hyg 95 :315–319.
-
10
Basco LK, Tahar R, Keundjian A, Ringwald P, 2000. Sequence variations in the genes encoding dihydropteroate synthase and dihydrofolate reductase and clinical response to sulfadoxine-pyrimethamine in patients with acute uncomplicated falciparum malaria. J Infect Dis 182 :624–628.
-
11
Wang P, Lee C-S, Bayoumi R, Djimde A, Doumbo O, Swedberg G, Dao LD, Mshinda H, Tanner M, Watkins MW, Sims PFG, Hyde JE, 1997. Resistance to antifolates in Plasmodium falciparum monitored by sequence analysis of dihydropteroate synthetase and dihydrofolate reductase alleles in a large number of field samples of diverse origins. Mol Biochem Parasitol 89 :161–177.
-
12
Plowe CV, Cortese JF, Djimde A, Nwanyanwu OC, Watkins WM, Winstanley PA, Estrada-Franco JG, Mollinedo RE, Avila JC, Cespedes JL, Carter D, Doumbo OK, 1997. Mutations in Plasmodium falciparum dihydrofolate reductase and dihydropteroate synthase and epidemiologic patterns of pyrimethamine-sulfadoxine use and resistance. J Infect Dis 176 :1590–1596.
-
13
Kublin JG, Dzinjalamala FK, Kamwendo DD, Malkin EM, Cortese JF, Martino LM, Mukadam RA, Rogerson SJ, Lescano AG, Molyneux ME, Winstanley PA, Chimpeni P, Taylor TE, Plowe CV, 2002. Molecular markers for failure of sulfadoxine-pyrimethamine and chlorproguanil-dapsone treatment of Plasmodium falciparum malaria. J Infect Dis 185 :380–388.
-
14
Rallon NI, Osorio LE, Giraldo LE, 1999. Lack of an association between the ASN-108 mutation in the dihydrofolate reductase gene and in vivo resistance to sulfadoxine/pyrimethamine in Plasmodium falciparum.Am J Trop Med Hyg 61 :245–248.
-
15
Kublin JG, Witzig RS, Shankar AH, Zurita JQ, Gilman RH, Guarda JA, Cortese JF, Plowe CV, 1998. Molecular assays for surveillance of antifolate-resistant malaria. Lancet 351 :1629–1630.
-
16
Khalil I, Alifrangis M, Ronn AM, Gabar HA, Jelinek T, Satti GM, Bygbjerg IC, 2002. Pyrimethamine/sulfadoxine combination in the treatment of uncomplicated falciparum malaria: relation between dihydropteroate synthase/dihydrofolate reductase genotypes, sulfadoxine plasma levels, and treatment outcome. Am J Trop Med Hyg 67 :225–229.
-
17
Nzila AM, Nduati E, Mberu EK, Hopkins SC, Monks SA, Winstanley PA, Watkins WM, 2000. Molecular evidence of greater selective pressure for drug resistance exerted by the long-acting antifolate pyrimethamine/sulfadoxine compared with the shorter-acting chlorproguanil/dapsone on Kenyan Plasmodium falciparum.J Infect Dis 181 :2023–2028.
-
18
Nagesha HS, Din S, Casey GJ, Susanti AI, Fryauff DJ, Reeder JC, Cowman AF, 2001. Mutations in the pfmdr1, dhfr and dhps genes of Plasmodium falciparum are associated with in-vivo drug resistance in West Papua, Indonesia. Trans R Soc Trop Med Hyg 95 :43–49.
-
19
WHO, 1973. Chemotherapy of malaria and resistance to antimalarial drugs. World Health Organ Tech Rep Ser 529.
-
20
WHO, 1996. Assessment of Therapeutic Efficacy of Antimalarial Drugs - For Uncomplicated Falciparum Malaria in Areas with Intense Transmission. Geneva: World Health Organization, WHO/MAL/96.1077.
-
21
Tarimo DS, Minjas JN, Bygbjerg IC, 2002. Sulfadoxine-pyrimethamine monotherapy in Tanzanian children gives rapid parasite clearance but slow fever clearance that is improved by chloroquine in combination therapy. Trop Med Int Health 7 :592–598.
-
22
Thompson R, Begtrup K, Cuamba N, Dgedge M, Mendis C, Gamage-Mendis A, Enosse SM, Barreto J, Sinden RE, Hogh B, 1997. The Matola malaria project: a temporal and spatial study of malaria transmission and disease in a suburban area of Maputo, Mozambique. Am J Trop Med Hyg 57 :550–559.
-
23
Lemnge MM, Msangeni HA, Rønn AM, Salum FM, Jakobsen PH, Mhina J, Akida JA, Bygbjerg IC, 1997. Maloprim malaria prophylaxis in children living in a holoendemic village in north-eastern Tanzania. Trans R Soc Trop Med Hyg 91 :68–73.
-
24
Sambrook J, Fritsch EF, Maniatis T, 1989. Molecular Cloning: A Laboratory Manual. Second edition. Cold Spring Harbor, NY: Cold Spring Harbor Laboratory Press.
-
25
Wooden J, Kyes S, Sibley CH, 1993. PCR and strain identification in Plasmodium falciparum.Parasitol Today 9 :303–305.
-
26
Duraisingh MT, Curtis J, Warhurst DC, 1998. Plasmodium falciparum: detection of polymorphisms in the dihydrofolate reductase and dihydropteroate synthetase genes by PCR and restriction digestion. Exp Parasitol 89 :1–8.
-
27
Jelinek T, Rønn AM, Lemnge MM, Curtis J, Mhina J, Duraisingh MT, Bygbjerg IC, Warhurst DC, 1998. Polymorphisms in dihydrofolate reductase (DHFR) and dihydropteroate synthetase (DHPS) genes of Plasmodium falciparum and in vivo resistance to sulfadoxine/pyrimethamine in isolates from Tanzania. Trop Med Int Health 3 :605–609.
-
28
Mutabingwa T, Nzila A, Mberu E, Nduati E, Winstanley P, Hills E, Watkins W, 2001. Chlorproguanil-dapsone for treatment of drug-resistant falciparum malaria in Tanzania. Lancet 358 :1218–1223.
-
29
Magesa SM, Mdira KY, Farnert A, Simonsen PE, Bygbjerg IC, Jakobsen PH, 2001. Distinguishing Plasmodium falciparum treatment failures from re-infections by using polymerase chain reaction genotyping in a holoendemic area in northeastern Tanzania. Am J Trop Med Hyg 65 :477–483.
| Past two years | Past Year | Past 30 Days | |
|---|---|---|---|
| Abstract Views | 20 | 20 | 7 |
| Full Text Views | 383 | 94 | 0 |
| PDF Downloads | 59 | 22 | 0 |