Log in

Relevant bibliographies by topics / Diminazeno / Journal articles

To see the other types of publications on this topic, follow the link: Diminazeno.

Journal articles on the topic 'Diminazeno'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the top 50 journal articles for your research on the topic 'Diminazeno.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Browse journal articles on a wide variety of disciplines and organise your bibliography correctly.

1

Seixas, Josilene N., Débora R. Orlando, Flademir Wouters, Angelica T. B. Wouters, Mary S. Varaschin, and Djeison L. Raymundo. "Aspectos patológicos da intoxicação por aceturato de diminazeno em camelídeos sul-americanos." Pesquisa Veterinária Brasileira 37, no. 12 (December 2017): 1509–13. http://dx.doi.org/10.1590/s0100-736x2017001200024.

Full text

Abstract:

RESUMO: Aceturato de diminazeno é um fármaco quimioterápico sintético comumente usado na medicina veterinária para o tratamento de doenças causadas por parasitos hematozoários. Entretanto, seu uso pode levar a efeitos colaterais, como alterações neurológicas graves e morte. A criação de camelídeos é uma atividade recente no Brasil, fazendo-se necessário conhecer mais sobre as doenças que acometem essas espécies. De dez camelídeos (seis lhamas e quatro alpacas) da propriedade, seis tiveram sinais clínicos e, destes, apenas uma lhama com manifestações leves recuperou-se. Os sinais clínicos incluíam apatia, andar cambaleante, fraqueza, sialorreia, cabeça baixa e pendida lateralmente, dificuldade em levantar e dispneia, observados a partir de 18 horas após o uso do medicamento. À necropsia e ao exame histopatológico foram observadas alterações de encefalopatia hemorrágica bilateral e simétrica, mais graves em tronco encefálico e tálamo. Este trabalho descreve as principais lesões observadas em um surto de intoxicação por diminazeno em alpacas (Lama pacos) e lhamas (Lama glama) e alerta criadores e veterinários sobre o risco de intoxicação por aceturato de diminazeno em camelídeos sul americanos.

APA, Harvard, Vancouver, ISO, and other styles

2

Silva, Aleksandro Schafer da, Camila Tochetto, Régis Adriel Zanette, Felipe Pierezan, Daniel Ricardo Rissi, Janio Morais Santurio, and Silvia Gonzalez Monteiro. "Aceturato de diminazeno e dipropionato de imidocarb no controle de infecção por Trypanosoma evansi em Rattus norvegicus infectados experimentalmente." Ciência Rural 38, no. 5 (August 2008): 1357–62. http://dx.doi.org/10.1590/s0103-84782008000500025.

Full text

Abstract:

Este estudo teve como objetivo avaliar o efeito do aceturato de diminazeno e do dipropionato de imidocarb no controle da infecção por Trypanosoma evansi em ratos (Rattus norvegicus) infectados experimentalmente. Cinqüenta e quatro ratos machos foram inoculados via intraperitonial com 104 tripomastigotas de T. evansi/animal. Os ratos foram monitorados diariamente por meio de esfregaço sanguíneo periférico. No momento em que se observassem oito protozoários por campo microscópico de 1000x, era iniciado o tratamento com as drogas (dia zero). O estudo foi dividido em dois protocolos terapêuticos e os fármacos foram administrados via intramuscular. O primeiro protocolo foi aplicado nos grupos A, B, C e D e o segundo protocolo nos grupos E, F, G e H. O grupo controle foi identificado como grupo I, não medicados. No primeiro protocolo, os ratos receberam uma dose única dos fármacos no dia zero e sempre que se observasse T. evansi na circulação periférica. No segundo protocolo, os roedores receberam as mesmas doses, no entanto, por cinco dias consecutivos. No primeiro protocolo, os dois princípios ativos não apresentaram eficácia curativa, ocorrendo reincidência da parasitemia após alguns dias do tratamento. No segundo protocolo, o aceturato de diminazeno eliminou a forma tripomastigota da circulação e os ratos foram eutanasiados após 90 dias do início do tratamento. Os roedores tratados com dipropionato de imidocarb apresentaram recidiva da infecção após 30 dias. Na histopatologia não se observou alteração renal e hepática relacionada à doença ou aos medicamentos testados. Com base nos resultados, foi concluído que o aceturato de diminazeno, quando administrado por cinco dias consecutivos, é efetivo no tratamento da tripanossomose em ratos.

APA, Harvard, Vancouver, ISO, and other styles

3

Flores, Mariana M., Paula R. Pereira, Alexandre Mazzanti, Glaucia D. Kommers, and Rafael A. Fighera. "Aspectos epidemiológicos, clínicos e anatomopatológicos da intoxicação por aceturato de diminazeno em cães." Pesquisa Veterinária Brasileira 34, no. 7 (July 2014): 667–74. http://dx.doi.org/10.1590/s0100-736x2014000700011.

Full text

Abstract:

Os aspectos epidemiológicos, clínicos e anatomopatológicos da intoxicação espontânea por aceturato de diminazeno foram estudados em 10 cães. Em todos os casos, os cães afetados demonstraram sinais de síndrome tálamo-cortical, principalmente alteração do nível de consciência, tetraparesia, rigidez extensora e crise convulsiva. Em alguns casos, os cães acometidos apresentaram sinais de síndrome cerebelar, como tremores musculares generalizados de alta frequência e baixa amplitude, e/ou de síndrome vestibular, como ataxia, inclinação de cabeça e quedas. Esses sinais ocorreram entre 24 e 48 horas após o uso do fármaco injetável por via intramuscular e se mantiveram até a morte ou eutanásia dos cães (entre 1 e 7 dias). Tais sinais clínicos refletiam encefalomalacia hemorrágica focal simétrica, que afetava a medula oblonga, a ponte, a medular do cerebelo, o tálamo, o mesencéfalo, os pedúnculos cerebelares e os núcleos da base. Esse artigo: 1) descreve e discute essa forma de intoxicação medicamentosa tão pouco citada na literatura internacional e desconhecida da maior parte dos clínicos e patologistas veterinários brasileiros, 2) estabelece critérios clínicos e anatomopatológicos para o seu diagnóstico e, principalmente, 3) atenta para os riscos da utilização desse princípio ativo na terapêutica canina.

APA, Harvard, Vancouver, ISO, and other styles

4

de Koning, Harry P., Laura F. Anderson, Mhairi Stewart, Richard J. S. Burchmore, Lynsey J. M. Wallace, and Michael P. Barrett. "The Trypanocide Diminazene Aceturate Is Accumulated Predominantly through the TbAT1 Purine Transporter: Additional Insights on Diamidine Resistance in African Trypanosomes." Antimicrobial Agents and Chemotherapy 48, no. 5 (May 2004): 1515–19. http://dx.doi.org/10.1128/aac.48.5.1515-1519.2004.

Full text

Abstract:

ABSTRACT Resistance to diminazene aceturate (Berenil) is a severe problem in the control of African trypanosomiasis in domestic animals. It has been speculated that resistance may be the result of reduced diminazene uptake by the parasite. We describe here the mechanisms by which [3H]diminazene is transported by Trypanosoma brucei brucei bloodstream forms. Diminazene was rapidly accumulated through a single transporter, with a Km of 0.45 ± 0.11 μM, which was dose dependently inhibited by pentamidine and adenosine. The Ki values for these inhibitors were consistent with this transporter being the P2/TbAT1 adenosine transporter. Yeast expressing TbAT1 acquired the ability to take up [3H]diminazene and [3H]pentamidine. TbAT1-null mutants had lost almost all capacity for [3H]diminazene transport. However, this cell line still displayed a small but detectable rate of [3H]diminazene accumulation, in a nonsaturable manner. We conclude that TbAT1 mediates [3H]diminazene transport almost exclusively and that this explains the observed diminazene resistance phenotypes of TbAT1-null mutants and field isolates.

APA, Harvard, Vancouver, ISO, and other styles

5

ANENE, B. M., R. C. EZEOKONKWO, T. I. MMESIRIONYE, J. N. A. TETTEY, J. M. BROCK, M. P. BARRETT, and H. P. DE KONING. "A diminazene-resistant strain of Trypanosoma brucei brucei isolated from a dog is cross-resistant to pentamidine in experimentally infected albino rats." Parasitology 132, no. 1 (September 12, 2005): 127–33. http://dx.doi.org/10.1017/s0031182005008760.

Full text

Abstract:

Trypanosomosis is a major cause of mortality for dogs in Nigeria and treatment with diminazene aceturate has steadily become less effective, either as a result of low quality of the locally available diminazene preparations or of drug resistance. To investigate these alternatives, samples of locally obtained drugs were analysed for diminazene aceturate content and a strain of Trypanosoma brucei brucei was isolated from a diminazene-refractory dog in Nsukka, south-eastern Nigeria, and used to infect albino rats. The quality of diminazene aceturate-based preparations was variable, with two preparations containing less than 95% of the stated active compound. Rats infected with T. brucei isolated from the dog were treated 7 and 10 days after infection either with 7 mg/kg diminazene aceturate (intraperitoneally, once) or with 4 mg/kg pentamidine isethionate (intramuscularly, 7 consecutive days). Relapse rates were 100% for both trypanocides in the groups of rat treated 10 days post-infection, and 83% and 50% of rats treated 7 days after infection relapsed to diminazene aceturate and pentamidine isethionate, respectively. Careful consideration of physiological parameters showed that pentamidine was only marginally superior to diminazene aceturate as applied in this study. It was concluded that dogs in Nigeria are infected with genuinely diminazene aceturate-resistant trypanosomes that appear to be cross-resistant to pentamidine isethionate.

APA, Harvard, Vancouver, ISO, and other styles

6

Eke, IG, UU Eze, IO Ezeh, TA Nzeakor, AO Anaga, and PA Onyeyili. "Effects of secnidazole-diminazene aceturate combination therapy on parasitaemia and serum biochemical profile after late treatment in Trypanosoma brucei brucei infected dogs." Veterinární Medicína 65, No. 12 (December 13, 2020): 543–52. http://dx.doi.org/10.17221/150/2019-vetmed.

Full text

Abstract:

Relapse parasitaemia is a major setback in the chemotherapy of a late stage Trypanosoma brucei brucei infection. An aberrant serum biochemical profile resulting from a T. b. brucei infection in dogs has been attributed to multiple organ injuries resulting from the invasive nature of the organism. Therapy with diminazene aceturate alone has not been satisfactory. This study evaluated the effects of a secnidazole-diminazine aceturate (SEC-DA) combination therapy on parasitaemia and the serum biochemical profile after the late treatment of a T. b. brucei infection in dogs. Eighteen dogs were randomly assigned to 6 groups (n = 3) as follows: Group A: uninfected nor treated; group B: infected without treatment; group C: infected and treated with DA (3.5 mg/kg) (DA-monotherapy) intramuscularly (i.m.) once; group D: infected and treated with SEC (100 mg/kg) and DA (3.5 mg/kg); group E: in-fected and treated with SEC (200 mg/kg) and DA (3.5 mg/kg) and group F: infected and treated with SEC (400 mg/kg) and DA (3.5 mg/kg). Secnidazole was administered orally for 5 days while DA was given i.m. once in groups D–F. The dogs were infected with 5 × 10<sup>5</sup> trypanosomes intraperitoneally and treatment started 14 days post-infection. The parasitaemia was monitored daily while the serum biochemical indicators were monitored 14, 21, and 28 days post-infection. The total aparasitaemia was achieved in the SEC-DA treated dogs 72 h post-treatment and in 86 h in the DA-monotherapy dogs. A relapse parasitaemia occurred in the DA-monotherapy dogs 17 days post-treatment. The SEC-DA combination therapy caused a significant (P < 0.05) decline in the hitherto elevated urea and creatinine concentrations, and the ALP, ALT, AST activities. Also, there was a significant (P < 0.05) increase in the previously decreased serum albumin in the SEC-DA treated dogs. In conclusion, secnidazole-diminazene aceturate combination therapy prevented the relapse parasitaemia and ameliorated aberrant serum biochemical profiles of T. b. brucei infected dogs after late treatment.

APA, Harvard, Vancouver, ISO, and other styles

7

Eke, I. G., U. U. Eze, T. A. Ezeudu, I. O. Ezeh, A. O. Anaga, and P. A. Onyeyili. "Diminazene aceturate residues in tissues of dogs treated with secnidazole-diminazene aceturate combination and with diminazene aceturate alone." Sokoto Journal of Veterinary Sciences 15, no. 4 (September 19, 2017): 16. http://dx.doi.org/10.4314/sokjvs.v15i4.3.

Full text

APA, Harvard, Vancouver, ISO, and other styles

8

Adeleye, Olushola Emmanuel, Jude Makinde Ale, Emmanuella Olubanke Amope Sogebi, Ladoke A. Durotoye, Adenike Iyabo Adeleye, Samuel Olufemi Adeyemi, and Johnny Olufemi Olukunle. "Effects of Trypanosoma brucei brucei infection and diminazene aceturate administration on the blood pressure, heart rate, and temperature of Wistar albino rats." Journal of Basic and Clinical Physiology and Pharmacology 29, no. 3 (June 27, 2018): 265–69. http://dx.doi.org/10.1515/jbcpp-2017-0201.

Full text

Abstract:

Abstract Background: This study was carried out to determine the blood pressure changes in experimentally Trypanosoma brucei brucei-infected Wistar albino rats and diminazene aceturate-treated rats. Methods: Twenty-four rats were purchased and divided into four groups consisting of six rats each. Control group (CON) received 0.5 mL of distilled water, i.m., infected but not treated group (INF) received 2×106 trypanosome/mL i.m., infected but diminazene aceturate-treated group (INFDIM) received 2×106 trypanosome/mL, 3.5 mg/kg, i.m.) and non-infected but diminazene aceturate-treated group (DIM) received 3.5 mg/kg, i.m. and served as negative control. The blood pressures were measured using a CODA 2® non-invasive blood pressure monitor (Kent Scientific, USA). The results were compiled and statistical analysis was done with significance set at p≥0.05. Results: The values of the blood pressure readings of the Trypanosoma-infected INF (137.0±2.0 mmHg) and diminazene-treated rats INFDIM (125.0±7.5 mmHg) when compared to the control group (168.0±3.0 mmHg) were significantly lower (p≤0.05) at the end of day 7. The heart rate was also significantly reduced in the INF (403.5±1.5 beats/min) and DIM (445.0±24 beats/min) groups of rats when compared with the control group (613.0±2.0 beats/min) at the end of day 8. Conclusion: The findings indicate the significant reduction in blood pressure and heart rates during Trypanosoma brucei brucei infection and with diminazene aceturate administration. Hence, caution should be exercised when treating trypanosome-infected patients with diminazene aceturate.

APA, Harvard, Vancouver, ISO, and other styles

9

Akode, Ruaa Mohamed, Shaza Wagiealla Shantier, Elrasheed Ahmed Gadkariem, and Magdi Awadalla Mohamed. "Simultaneous Determination and Stability Studies on Diminazene Diaceturate and Phenazone Using Developed Derivative Spectrophotometric Method." International Journal of Analytical Chemistry 2017 (2017): 1–6. http://dx.doi.org/10.1155/2017/4269587.

Full text

Abstract:

This work presents UV first derivative spectrophotometry as a precise, accurate, and feasible method for simultaneous determination of diminazene diaceturate and phenazone in bulk and dosage forms. The absorbance values of diminazene diaceturate and phenazone aqueous mixture were obtained at 398 nm and 273 nm, respectively. The developed method was proved to be linear over the concentration ranges (2–10) μg/mL and (2.496–12.48) μg/mL for diminazene diaceturate and phenazone, respectively, with good correlation coefficients (not less than 0.997). The detection and quantitation limits were found to be (LOD = 0.63 and 0.48 μg/mL; LOQ = 1.92 and 1.47 μg/mL, resp.). The developed method was employed for stability studies of both drugs under different stress conditions. Diminazene diaceturate was prone to degrade at acidic pH via first-order kinetics. The degradation process was found to be temperature dependent with an activation energy of 7.48 kcal/mole. Photo-stability was also investigated for this drug.

APA, Harvard, Vancouver, ISO, and other styles

10

Burudi, E. M. E., A. S. Peregrine, P. A. O. Majiwa, S. M. Mbiuki, and N. B. Murphy. "Response of diminazene-resistant and diminazene-susceptibleTrypanosoma congolenseto treatment with diminazene when occurring as a mixed infection in goats." Annals of Tropical Medicine & Parasitology 88, no. 6 (January 1994): 595–606. http://dx.doi.org/10.1080/00034983.1994.11812910.

Full text

APA, Harvard, Vancouver, ISO, and other styles

11

Jolayemi, KO, M. Mamman, D. Sani, M. O. Okoronkwo, and J. Amaje. "In vitro and in vivo changes observed in Trypanosoma brucei brucei-infected rats treated with artesunate and/or diminazene aceturate." Sokoto Journal of Veterinary Sciences 18, no. 4 (February 18, 2021): 211–20. http://dx.doi.org/10.4314/sokjvs.v18i4.5.

Full text

Abstract:

This study evaluated in vitro and in vivo antitrypanosomal effect of artesunate and/or diminazene aceturate in Wistar rats experimentally infected with Trypanosoma brucei brucei. In vitro screening was carried out in triplicates using 50 μl of 0.2, 2 and 20 μg/μl of artesunate as test drug; diminazene aceturate, normal saline and trypanosome-infected blood served as controls in a 96-well microtitre plate, incubated at 37˚C for 5 minutes. Efficacy was observed over a period of 60 minutes for reduced or complete trypanosomal immobilization. Results showed concentration-dependent cessation of trypanosomal motility was significantly (p < 0.001) induced by artesunate when compared to the controls. Seventy Wistar rats of both sexes weighing between 190 and 210 g were randomly divided into 7 groups (5 males and 5 females) are used for in vivo study. Groups I and II served as normal control and model control respectively. Groups III to VII were infected with Trypanosoma brucei brucei (106 trypanosomes/ml) intraperitoneally. At peak parasitaemia (8 days post-infection), group III was treated with diminazene aceturate (3.5 mg/kg) intramuscularly once while groups IV, V, VI were treated with artesunate (200, 100, 50) mg/kg orally for 5 consecutive days and group VII was treated with combination of artesunate (50 mg/kg) orally and diminazene aceturate (1.75 mg/kg) intramuscularly for 5 days. Results indicated pre-patent period of 4 days and increase in levels of parasitaemia post-inoculation. PCV, Hb concentration, RBC count, MCV, MCHC and total leucocyte count decreased significantly (p < 0.05) between days 0and 8 in groups II to VII. Following treatment, significant increases (p < 0.05) were recorded except for groups II, IV, V and VI where the rats died. Thus, combination of artesunate (50 mg/kg) and half the standard dose of diminazene aceturate was able to reduce parasitaemia and ameliorate the anaemia elicited by the trypanosomes. Keywords: Artesunate, Diminazene Aceturate, Haematology, Trypanosoma brucei brucei, Wistar rats

APA, Harvard, Vancouver, ISO, and other styles

12

Anya, D. K., and K. I. Eghianruwa. "Concurrent administration of methanolic extract of Zingiber officinale Roscoe (Zingiberales: Zingiberaceae) and diminazene aceturate enhanced survival rate and reduced parasitaemia in experimental murine Trypanosoma brucei Plimmer & Bradford, 1899 (Kinetoplastea: Trypanosomatida) infection." Brazilian Journal of Biological Sciences 5, no. 9 (2018): 95–104. http://dx.doi.org/10.21472/bjbs.050910.

Full text

Abstract:

The efficacy of concurrent diminazene and Zingiber officinale Roscoe (Zingiberales: Zingiberaceae) extract in murine Trypanosoma brucei Plimmer & Bradford, 1899 (Kinetoplastea: Trypanosomatida) infection was evaluated. Two infected groups were treated with extract at 400 mg.kg-1 (G1) and 800 mg.kg-1 (G2) alone while another two groups received 400 mg.kg-1 (GD1) and 800 mg.kg-1 (GD2) of extract concurrently with diminazene 3.5 mg.kg-1 intraperitoneally. One infected group received diminazene 3.5 mg.kg-1 only (D) while another received 1 mg.kg-1 Tween 80 (C1) orally. The seventh group was uninfected and untreated (C2). Survival rate, parasitemia, liver weight, spleen weight, haematological indices were evaluated. Survival rates were 0% in C1, G1 and G2, 20% in D, 40% in GD2, 60% in GD1 and 100% in C2. Animals in groups G1, G2 and C1 died between 6 and 8 days pt. Parasitemia levels were significantly (P < 0.05) higher in D1 than in GD1 and GD2 by day 16 post treatment. PCV and RBC counts were significantly (P < 0.05) lower in GD1, GD2 and D than in C2. Liver and spleen weights increased significantly (P < 0.05) due to infection and never fully recovered in all treatment options. Ginger (Z. officinale) extract enhanced diminazene efficacy by increasing survival rates and lowering parasitemia.

APA, Harvard, Vancouver, ISO, and other styles

13

Amuzescu, Bogdan P., Thomas Knott, Olaf Scheel, Dan Mihailescu, and Maria Mernea. "Diminazene Interaction with ASIC1A Channels." Biophysical Journal 106, no. 2 (January 2014): 550a. http://dx.doi.org/10.1016/j.bpj.2013.11.3062.

Full text

APA, Harvard, Vancouver, ISO, and other styles

14

Aliu, Y. Otaru, and Stig Ødegaard. "Pharmacokinetics of diminazene in sheep." Journal of Pharmacokinetics and Biopharmaceutics 13, no. 2 (April 1985): 173–84. http://dx.doi.org/10.1007/bf01059397.

Full text

APA, Harvard, Vancouver, ISO, and other styles

15

Peregrine, A. S., and M. Mamman. "Pharmacology of diminazene: a review." Acta Tropica 54, no. 3-4 (September 1993): 185–203. http://dx.doi.org/10.1016/0001-706x(93)90092-p.

Full text

APA, Harvard, Vancouver, ISO, and other styles

16

Peregrine, A. S., G. Knowles, A. I. Ibitayo, J. R. Scott, S. K. Moloo, and N. B. Murphy. "Variation in resistance to isometamidium chloride and diminazene aceturate by clones derived from a stock ofTrypanosoma congolense." Parasitology 102, no. 1 (February 1991): 93–100. http://dx.doi.org/10.1017/s0031182000060388.

Full text

Abstract:

SUMMARYNine clones were derived from a drug-resistantTrypanosoma congolensestock (IL 2856) and characterized in mice for their sensitivity to isometamidium chloride and diminazene aceturate. All clones were derived from the stock without drug selection and expressed high levels of resistance to isometamidium chloride (50% curative dose [CD50] values ranging from 1·5 to 5·1 mg/kg) and intermediate to high levels of resistance to diminazene aceturate (CD50values ranging from 5·1 to 21·0 mg/kg). By contrast, the isometamidium chloride and diminazene aceturate CD50values for a drug-sensitive clone,T. congolenseIL 1180, were 0·018 mg/kg and 2·3 mg/kg, respectively. For both drugs, there appeared to be significantly different levels in expression of drug resistance amongst the 9 clones derived from IL 2856. Isoenzyme analysis of 7 enzymes showed that all 9 clones expressed the same electrophoretic variants. Thus, all 9 clones were identical for these phenotypic markers. The clone which expressed the highest level of resistance to isometamidium in mice (IL 3270) was transmitted to Boran cattle via the bite of infectedGlossina morsitans centralis. IL 3270 produced an infection rate in tsetse of 5·0%. The resulting infections in cattle were shown to be resistant to intramuscular treatment with 2·0 mg/kg isometamidium chloride and 14·0 mg/kg diminazene aceturate. This contrasts with doses of 0·25 mg/kg isometamidium chloride or 3·5 mg/kg diminazene aceturate which are deemed sufficient to cure fully sensitive infections. Finally, 9 clones (subclones) were derived from IL 3270 and characterized in mice for their sensitivity to isometamidium chloride. Seven of the subclones expressed a significantly lower level of resistance to isometamidium than the parental clone and amongst the subclones there was significant variation in resistance. Thus, expression of a high level of resistance to isometamidium appears to be unstable in the rodent host and at least a component of the genetic determinant(s) for this drug-resistant phenotype is (are) likely to be unstable.

APA, Harvard, Vancouver, ISO, and other styles

17

Rashid, Hamad Bin, Mamoona Chaudhry, Haroon Rashid, Khalid Pervez, Muhammad Arif Khan, and Asim Khalid Mahmood. "Comparative efficacy of diminazene diaceturate and diminazene aceturate for the treatment of babesiosis in horses." Tropical Animal Health and Production 40, no. 6 (December 15, 2007): 463–67. http://dx.doi.org/10.1007/s11250-007-9121-2.

Full text

APA, Harvard, Vancouver, ISO, and other styles

18

Othman, T. "THE TOXIC EFFECTS OF MULTIPLE DOSES OF DIMINAZENE ACETURATE ON THE HAEMATOLOGICAL VALUES OF RATS." Nigerian Journal of Animal Production 21 (January 3, 2021): 146–48. http://dx.doi.org/10.51791/njap.v21i1.1168.

Full text

Abstract:

The haematological effects of increasing doses of diminazene aceturate on the blood of swiss albino rats was examined. Following the administration of the drug there was a significant increase in white blood cell (WBC) count (P<0.05). The increase in WBC count occured at all dose levels of 3.5, 7.0), 14.0 and 28.0mg/kg body weight. There was minor change in serum sodium and significant changes in serum potassium levels. All these changes were found not to be strictly dose dependent. This study shows that administration of diminazene aceturate produces increases in white blood cells.

APA, Harvard, Vancouver, ISO, and other styles

19

Oyewusi, I. K., M. I. Takeet, A. J. Oyewusi, A. O. Talabi, A. O. Sonibare, and E. B. Otesile. "Response of Three Nigerian Breeds of Sheep Experimentally Infected with Trypanosoma vivax to Diminazene Aceturate Therapy." Folia Veterinaria 64, no. 3 (September 1, 2020): 13–21. http://dx.doi.org/10.2478/fv-2020-0022.

Full text

Abstract:

AbstractThe efficacy of diminazene aceturate in three Nigerian breeds of sheep [West African Dwarf (WAD), Yankassa and Ouda] experimentally infected with Trypanosoma vivax was studied. Five rams of each breed were administered 0.5 ml of goat blood containing 2.5 × 106T. vivax per millilitre intravenously, while three rams of each breed served as uninfected controls. The treatment with diminazene aceturate was intramuscularly administered to the infected sheep, when their packed cell volume (PCV) fell to 15 %, at a dosage of 7 mg.kg−1 b. w. The parameters measured were parasitaemia, live weight gain and PCV. By 24 hours post treatment (pt.), no trypanosomes were detected by either the Haematocrit Concentration Technique (HCT) or the Polymerase Chain Reaction (PCR) in the blood of any of the treated sheep. However, a relapse of parasitaemia occurred 17 to 32 days pt. in 46.7 % of the treated rams and these were retreated with 14 mg.kg−1 b. w. diminazene aceturate. There were gradual increments in the live weight gain and the PCV of the treated rams until the resurgence of parasitaemia. Ouda had the highest cases of relapse (80 %), the least mean live weight gain and was the only breed in which mortality was recorded despite the treatment. In conclusion, diminazene aceturate administered at 7 mg.kg−1 b. w. cleared the trypanosomes in the blood of all the treated sheep within 24 hours and this was accompanied by the restoration of lost weight and the reversal of anaemia. However, the subsequent resurgence of parasitaemia indicated that a dosage of 7 mg.kg−1 b. w. was no longer reliable for complete elimination of trypanosomes from all the tissues of the host.

APA, Harvard, Vancouver, ISO, and other styles

20

Zaazaa, Hala E., Nahla N. Salama, Shereen M. Azab, Shimaa A. Atty, Naglaa M. El-Kosy, and Maissa Y. Salem. "A novel surfactant silica gel modified carbon paste electrode in micellar media for selective determination of diminazene aceturate in the presence of its stabilizer." RSC Advances 5, no. 60 (2015): 48842–50. http://dx.doi.org/10.1039/c5ra06292f.

Full text

APA, Harvard, Vancouver, ISO, and other styles

21

Velkoska, Elena, Sheila K. Patel, and Louise M. Burrell. "Angiotensin converting enzyme 2 and diminazene." Current Opinion in Nephrology and Hypertension 25, no. 5 (September 2016): 384–95. http://dx.doi.org/10.1097/mnh.0000000000000254.

Full text

APA, Harvard, Vancouver, ISO, and other styles

22

Yamasaki, Masahiro, Nao Watanabe, Natsuki Idaka, Tohru Yamamori, Ken-ichi Otsuguro, Naohiro Uchida, Aiko Iguchi, Hiroshi Ohta, and Mitsuyoshi Takiguchi. "Intracellular diminazene aceturate content and adenosine incorporation in diminazene aceturate-resistant Babesia gibsoni isolate in vitro." Experimental Parasitology 183 (December 2017): 92–98. http://dx.doi.org/10.1016/j.exppara.2017.10.016.

Full text

APA, Harvard, Vancouver, ISO, and other styles

23

Mamoudou, A., A. Zoli, C. Tanenbe, J. P. Andrikaye, Mr Bourdanne, Tanguy Marcotty, V. Delespaux, Peter-Henning Clausen, and S. Geerts. "Evaluation sur le terrain et sur souris de la résistance des trypanosomes des bovins du plateau de l’Adamaoua au Cameroun à l’acéturate de diminazène et au chlorure d’isométamidium." Revue d’élevage et de médecine vétérinaire des pays tropicaux 59, no. 1-4 (January 1, 2006): 11. http://dx.doi.org/10.19182/remvt.9948.

Full text

Abstract:

Suite à une enquête dans quelques villages du département de Faro et Déo, le village de Kontcha, qui a présenté la prévalence de la trypanosomose la plus élevée (32,5 p. 100), a été sélectionné afin d’évaluer la résistance des trypanosomes au diminazène et à l’isométamidium. Deux lots de 40 bovins ont été traités au jour 0, l’un au diminazène, l’autre à l’isométamidium. Le statut parasitologique de ces deux lots a été évalué toutes les deux semaines en utilisant la technique du buffy coat pendant une période de deux mois. Chaque animal diagnostiqué positif a été traité au diminazène. Le pourcentage d’animaux infectés par des trypanosomes a été de 32,5 p. 100 dans le lot traité au diminazène et de 27,5 p. 100 dans le lot traité à l’isométamidium. L’analyse de survie ainsi que l’estimation du risque relatif (1,38) ont suggéré une résistance à l’isométamidium et une diminution de l’activité prophylactique de ce produit. Plusieurs animaux traités au diminazène à 7 mg/kg ont été diagnostiqués positifs deux semaines après le traitement, ce qui indiquait également une forte suspicion de résistance à ce trypanocide. Ces résultats du terrain ont été confirmés par le test standardisé sur souris en utilisant six isolats de Trypanosoma congolense provenant des animaux traités. Ces isolats ont été testés au chlorure d’isométamidium (1 mg/kg) et à l’acéturate de diminazène (20 mg/kg) pour établir leur sensibilité. Tous les isolats ont été résistants à au moins un des produits testés, tandis que quatre isolats ont été résistants aux deux produits. Cette étude montre pour la première fois la présence au Cameroun de souches de trypanosomes résistantes aux trypanocides.

APA, Harvard, Vancouver, ISO, and other styles

24

Souza, Luan Kelves Miranda de, Kerolayne de Melo Nogueira, and Jand Venes Rolim Medeiros. "Technological prospection of Diminazene Aceturate, an Angiotensin II Converting Enzyme activator, in front of diarrheic disorders." Research, Society and Development 9, no. 12 (December 11, 2020): e1691210755. http://dx.doi.org/10.33448/rsd-v9i12.10755.

Full text

Abstract:

Diarrhea, which is a gastrointestinal disease, has as its main characteristic the rapid passage of gastric contents through the intestine, which leads to the loss of water and electrolytes and consequent dehydration. The most common fluid replacement is the use of oral rehydration solution (ORS) together with the use of the drug loperamide. However, the use of this medication can cause severe bacteremia followed by sepsis and even death. Currently, there is no effective pharmacological treatment for diarrhea, therefore, it is noted the importance of seeking new therapeutic targets for the treatment of this disease. Thus, the aim of the present study was to conduct a research on the biological activities already described for Diminazene Aceturate with a special focus on antidiarrheal agents. For this, a survey was carried out, through patent filing searches, in the USPTO, EPO, WIPO and INPI databases, using keywords and Boolean operators. Thus, it was found in the international patent databases the number of documents referring to the use of Diminazene Aceturate in several areas, mainly in the pharmaceutical industry, but with a relatively low number of documents regarding the description of possible antidiarrheal action of the compound under study , which reinforces the innovative character of research involving the use of Diminazene Aceturate as an antidiarrheal agent.

APA, Harvard, Vancouver, ISO, and other styles

25

Stewart, Mhairi L., Richard J. S. Burchmore, Caroline Clucas, Christiane Hertz-Fowler, Karen Brooks, A. Tait, A. MacLeod, et al. "Multiple Genetic Mechanisms Lead to Loss of Functional TbAT1 Expression in Drug-Resistant Trypanosomes." Eukaryotic Cell 9, no. 2 (December 4, 2009): 336–43. http://dx.doi.org/10.1128/ec.00200-09.

Full text

Abstract:

ABSTRACT The P2 aminopurine transporter, encoded by TbAT1 in African trypanosomes in the Trypanosoma brucei group, carries melaminophenyl arsenical and diamidine drugs into these parasites. Loss of this transporter contributes to drug resistance. We identified the genomic location of TbAT1 to be in the subtelomeric region of chromosome 5 and determined the status of the TbAT1 gene in two trypanosome lines selected for resistance to the melaminophenyl arsenical, melarsamine hydrochloride (Cymelarsan), and in a Trypanosoma equiperdum clone selected for resistance to the diamidine, diminazene aceturate. In the Trypanosoma brucei gambiense STIB 386 melarsamine hydrochloride-resistant line, TbAT1 is deleted, while in the Trypanosoma brucei brucei STIB 247 melarsamine hydrochloride-resistant and T. equiperdum diminazene-resistant lines, TbAT1 is present, but expression at the RNA level is no longer detectable. Further characterization of TbAT1 in T. equiperdum revealed that a loss of heterozygosity at the TbAT1 locus accompanied loss of expression and that P2-mediated uptake of [3H]diminazene is lost in drug-resistant T. equiperdum. Adenine-inhibitable adenosine uptake is still detectable in a ΔTbat1 T. b. brucei mutant, although at a greatly reduced capacity compared to that of the wild type, indicating that an additional adenine-inhibitable adenosine permease, distinct from P2, is present in these cells.

APA, Harvard, Vancouver, ISO, and other styles

26

Mamman, M., D. J. L. Williams, N. B. Murphy, and A. S. Peregrine. "Apparent rarity of diminazene-resistant trypanosomes in goats infected with a diminazene-resistant population of Trypanosoma congolense." Research in Veterinary Science 58, no. 2 (March 1995): 113–18. http://dx.doi.org/10.1016/0034-5288(95)90062-4.

Full text

APA, Harvard, Vancouver, ISO, and other styles

27

S. Chigozie, U., A. B. Maduka, and J. G. Ifeanyi. "Trypanocidal efficacy of diminazene in diabetic rats." Iraqi Journal of Veterinary Sciences 26, no. 1 (June 28, 2012): 33–38. http://dx.doi.org/10.33899/ijvs.2012.46950.

Full text

APA, Harvard, Vancouver, ISO, and other styles

28

LEWIS, K. M., L. A. COHN, A. J. BIRKENHEUER, and M. G. PAPICH. "Pharmacokinetics of diminazene diaceturate in healthy cats." Journal of Veterinary Pharmacology and Therapeutics 35, no. 6 (December 29, 2011): 608–10. http://dx.doi.org/10.1111/j.1365-2885.2011.01359.x.

Full text

APA, Harvard, Vancouver, ISO, and other styles

29

Fraga-Silva, R., F. Montecucco, F. P. Costa-Fraga, F. Mach, R. A. S. Santos, R. F. Silva, and N. Stergiopulos. "Diminazene enhances stable phenotype of atherosclerotic plaques." Atherosclerosis 241, no. 1 (July 2015): e45. http://dx.doi.org/10.1016/j.atherosclerosis.2015.04.162.

Full text

APA, Harvard, Vancouver, ISO, and other styles

30

Zhou, Jie, Vu Le, Dimpy Kalia, Shizuka Nakayama, Clinton Mikek, Edwin A. Lewis, and Herman O. Sintim. "Diminazene or berenil, a classic duplex minor groove binder, binds to G-quadruplexes with low nanomolar dissociation constants and the amidine groups are also critical for G-quadruplex binding." Mol. BioSyst. 10, no. 10 (2014): 2724–34. http://dx.doi.org/10.1039/c4mb00359d.

Full text

APA, Harvard, Vancouver, ISO, and other styles

31

Tuvshintulga, Bumduuren, Mahmoud AbouLaila, Batdorj Davaasuren, Aki Ishiyama, Thillaiampalam Sivakumar, Naoaki Yokoyama, Masato Iwatsuki, Kazuhiko Otoguro, Satoshi Ōmura, and Ikuo Igarashi. "Clofazimine Inhibits the Growth of Babesia and Theileria ParasitesIn VitroandIn Vivo." Antimicrobial Agents and Chemotherapy 60, no. 5 (February 16, 2016): 2739–46. http://dx.doi.org/10.1128/aac.01614-15.

Full text

Abstract:

ABSTRACTThe present study evaluated the growth-inhibitory effects of clofazimine, currently used for treating leprosy, againstBabesia bovis,B. bigemina,B. caballi, andTheileria equiinin vitroculture and againstBabesia microtiin mice. The 50% inhibitory concentrations (IC50s) of clofazimine against thein vitrogrowth ofB. bovis,B. bigemina,B. caballi, andT. equiwere 4.5, 3, 4.3, and 0.29 μM, respectively. In mice infected withB. microti, treatment with 20 mg/kg of body weight of clofazimine administered orally resulted in a significantly lower peak parasitemia (5.3%) than that in the control group (45.9%), which was comparable to the subcutaneous administration of 25 mg/kg diminazene aceturate, the most widely used treatment for animal piroplasmosis. Although slight anemia was observed in both clofazimine- and diminazene aceturate-treated infected mice, the level and duration of anemia were lower and shorter, respectively, than those in untreated infected mice. Using blood transfusions and PCR, we also examined whether clofazimine completely killedB. microti. On day 40 postinfection, when blood analysis was performed, parasites were not found in blood smears; however, the DNA ofB. microtiwas detected in the blood of clofazimine-treated animals and in several tissues of clofazimine- and diminazene aceturate-treated mice by PCR. The growth of parasites was observed in mice after blood transfusions from clofazimine-treated mice. In conclusion, clofazimine showed excellent inhibitory effects againstBabesiaandTheileria in vitroandin vivo, and further study on clofazimine is required for the future development of a novel chemotherapy with high efficacy and safety against animal piroplasmosis and, possibly, human babesiosis.

APA, Harvard, Vancouver, ISO, and other styles

32

Dwivedi, Varsha, Archana Ayyagari, Rakhi Chandran, Prerna Diwan, Sanjay Gupta, and Vandana Gupta. "Repurposing Potential of Diminazene Aceturate as an Inhibitor of the E. coli DNA Gyrase B." Journal of Biomedical Research & Environmental Sciences 1, no. 6 (October 2020): 263–70. http://dx.doi.org/10.37871/jbres1153.

Full text

Abstract:

Drug-resistant Escherichia coli (E. coli) has overburdened the healthcare facilities in recent years and is getting hard to combat, mandating search for novel therapeutics with a broad antibacterial spectrum and high chemotherapeutic index. The 24 kDa domain of DNA gyrase B that is involved in the ATPase activity has been reported to be a promising target for inhibitors. A PDB structure (1KZN) of the 24kD domain of gyrase B with the co-crystallized ligand clorobiocin was used for the docking studies to explore a library of 2924 FDA approved drugs from www.zinc.docking.org. FlexX docking module from Biosolve IT was used for receptor preparation and in silico docking experiments. Docking studies on the pocket created around the reference ligand clorobiocin revealed the best score with diminazene aceturate and it also demonstrated interactions with the crucial amino acids present within the pocket. Diminazene aceturate has been conventionally been used as an antiparasitic molecule in animals and it has also been demonstrated to exhibit repurposing potential in the treatment of disorders triggered due to overproduction of inflammatory cytokines, pulmonary hypertension, ischemia-induced cardiac pathophysiology, etc. among others. Findings from this study indicate the possibility of repurposing the age-old molecule diminazene aceturate into a DNA gyrase B antagonist to combat not just the drug-resistant E. coli but also other gram-negative ESKAPE pathogens. It may also aid in alleviating the inflammatory response induced in the body of the patients suffering from septicemia caused by a variety of Gram-negative bacterial pathogens.

APA, Harvard, Vancouver, ISO, and other styles

33

Guswanto, Azirwan, Thillaiampalam Sivakumar, Mohamed Abdo Rizk, Shimaa Abd Elsalam Elsayed, Mohamed Ahmed Youssef, ElSaid El Shirbini ElSaid, Naoaki Yokoyama, and Ikuo Igarashi. "Evaluation of a Fluorescence-Based Method for Antibabesial Drug Screening." Antimicrobial Agents and Chemotherapy 58, no. 8 (June 9, 2014): 4713–17. http://dx.doi.org/10.1128/aac.00022-14.

Full text

Abstract:

ABSTRACTIn vitroevaluation of chemotherapeutic agents againstBabesiaandTheileriaparasites has become routine, and the effectiveness of these chemicals is usually determined by comparing the parasitemia dynamics of untreated and treated parasites. Although microscopy is widely used to calculate parasitemia, several disadvantages are associated with this technique. The present study evaluated a fluorescence-based method using SYBR green I stain (SG I) to screen antibabesial agents inin vitrocultures ofBabesia bovis. The linearity between relative fluorescence units (RFU) and parasitemia was found to be well correlated with a 0.9944 goodness-of-fit (r2) value. Subsequently, 50% inhibitory concentration (IC50) values were calculated for 3 antiprotozoan agents, diminazene aceturate, nimbolide, and gedunin, by this method. For diminazene aceturate and nimbolide, the IC50s determined by the fluorescence-based method (408 nM and 8.13 μM, respectively) and microscopy (400.3 nM and 9.4 μM, respectively) were in agreement. Furthermore, the IC50of gedunin determined by the fluorescence-based method (19 μM) was similar to the recently described microscopy-based value (21.7 μM) forB. bovis. Additionally, the Z′ factor (0.80 to 0.90), signal-to-noise (S/N) ratio (44.15 to 87.64), coefficient of variation at the maximum signal (%CVmax) (0.50 to 2.85), and coefficient of variation at the minimum signal (%CVmin) (1.23 to 2.21) calculated for the fluorescence method using diminazene aceturate were comparable to those previously determined in malaria research for this assay. These findings suggest that the fluorescence-based method might be useful for antibabesial drug screening and may have potential to be developed into a high-throughput screening (HTS) assay.

APA, Harvard, Vancouver, ISO, and other styles

34

Mamman, M., G. Gettinby, N. B. Murphy, S. Kemei, and A. S. Peregrine. "Frequency of diminazene-resistant trypanosomes in populations of Trypanosoma congolense arising in infected animals following treatment with diminazene aceturate." Antimicrobial Agents and Chemotherapy 39, no. 5 (May 1, 1995): 1107–13. http://dx.doi.org/10.1128/aac.39.5.1107.

Full text

APA, Harvard, Vancouver, ISO, and other styles

35

Dargantes, Alan P., April Hari Wardhana, Jose Alexander C. Abella, Milkesidick R. Sequito, Simon A. Reid, Douglas Bruce Copeman, and K. AT Dargantes. "Pathogenicity of Philippine and Indonesian Trypanosoma evansi Isolates in Mice and Their Responses to Trypanocides." Jurnal Ilmu Ternak dan Veteriner 26, no. 1 (June 22, 2021): 22. http://dx.doi.org/10.14334/jitv.v26i1.2508.

Full text

Abstract:

Pathogenicity of 10 isolates of <em>T. evansi</em> collected from Mindanao, Philippines, and one isolate from East Java, Indonesia was determined and compared. The susceptibility of these isolates against diminazene aceturate, melarsomine dihydrochloride, suramin and quinapyramine sulphate/chloride was also tested. Twenty-five mice were infected intraperitoneally with each isolate and 20 were treated with the 4 drugs (5 mice/drug) while 5 infected and 7 uninfected mice served as infected-untreated and uninfected controls, respectively. Treatment was carried out 24 hours post-infection and parasitemia was monitored for 35 days. Mice infected with Philippine isolates significantly died earlier (5-11 days) than those infected with the Indonesian isolate (14-16 days). The prepatent period for Philippine isolates (3-8 days) was significantly shorter than the Indonesian strain (11-13 days). Trypanosomes were not observed in the blood of mice infected with any of the Philippine isolates when treated with quinapyramine sulphate/chloride, melarsomine dihydrochloride or suramin. Two of 10 mice infected with either C4 or A9 Philippine isolates and treated with diminazene aceturate had parasitemia on days 29 and 31, respectively. It is concluded that isolates of <em>T. evansi</em> from Mindanao, Philippines, are more pathogenic than the isolate from East Java, Indonesia. This study also indicated that quinapyramine sulphate/chloride, melarsomine dihydrochloride and suramin are effective against these <em>T. evansi</em> isolates from Mindanao, Philippines and East Java, Indonesia, while two of the Mindanao isolates are resistant to diminazene. This information is valuable in the enhancement of the control strategy against surra in the Philippines and Indonesia.

APA, Harvard, Vancouver, ISO, and other styles

36

Karanja, Wycliff M., Raymond E. Mdachi, and Grace A. Murilla. "A competitive enzyme-linked immunosorbent assay for diminazene." Acta Tropica 84, no. 2 (November 2002): 75–81. http://dx.doi.org/10.1016/s0001-706x(02)00184-5.

Full text

APA, Harvard, Vancouver, ISO, and other styles

37

Fraga‐Silva, Rodrigo A., Fabiana P. Costa‐Fraga, Fabrizio Montecucco, Mikael Sturny, Younoss Faye, François Mach, Graziano Pelli, et al. "Diminazene Protects Corpus Cavernosum Against Hypercholesterolemia‐Induced Injury." Journal of Sexual Medicine 12, no. 2 (February 2015): 289–302. http://dx.doi.org/10.1111/jsm.12757.

Full text

APA, Harvard, Vancouver, ISO, and other styles

38

Rigatto, Katya, Karina R. Casali, Vinayak Shenoy, Michael J. Katovich, and Mohan K. Raizada. "Diminazene aceturate improves autonomic modulation in pulmonary hypertension." European Journal of Pharmacology 713, no. 1-3 (August 2013): 89–93. http://dx.doi.org/10.1016/j.ejphar.2013.04.017.

Full text

APA, Harvard, Vancouver, ISO, and other styles

39

Mamman, M., Y. O. Aliu, and A. S. Peregrine. "Pharmacokinetics of diminazene in female boran (bos indicus) cattle." European Journal of Pharmacology 183, no. 5 (July 1990): 1866. http://dx.doi.org/10.1016/0014-2999(90)92200-3.

Full text

APA, Harvard, Vancouver, ISO, and other styles

40

Banna, H. A. El, K. Abo El-Sooud, and G. A. Soliman. "Comparative Pharmacokinetics of Diminazene in Lactating Goats and Sheep." Journal of Veterinary Medicine Series A 46, no. 1 (February 1999): 49–58. http://dx.doi.org/10.1046/j.1439-0442.1999.00191.x.

Full text

APA, Harvard, Vancouver, ISO, and other styles

41

Campbell, Michael, Richard J. Prankerd, Ashley S. Davie, and William N. Charman. "Degradation of berenil (diminazene aceturate) in acidic aqueous solution." Journal of Pharmacy and Pharmacology 56, no. 10 (October 2004): 1327–32. http://dx.doi.org/10.1211/0022357044409.

Full text

APA, Harvard, Vancouver, ISO, and other styles

42

ALIU, Y. O., M. MAMMAN, and A. S. PEREGRINE. "Pharmacokinetics of diminazene in female Boran (Bos indicus) cattle." Journal of Veterinary Pharmacology and Therapeutics 16, no. 3 (September 1993): 291–300. http://dx.doi.org/10.1111/j.1365-2885.1993.tb00176.x.

Full text

APA, Harvard, Vancouver, ISO, and other styles

43

Yoshimura, H. "Teratological assessment of the antiprotozoal, diminazene diaceturate, in rats." Toxicology Letters 54, no. 1 (November 1990): 55–59. http://dx.doi.org/10.1016/0378-4274(90)90055-q.

Full text

APA, Harvard, Vancouver, ISO, and other styles

44

Chao, Mengjia, Xinxin Xu, Liqiang Liu, Aihong Wu, Shanshan Song, Hua Kuang, and Chuanlai Xu. "Ultrasensitive immunochromatographic strip assay for the detection of diminazene." Analyst 146, no. 15 (2021): 4927–33. http://dx.doi.org/10.1039/d1an00908g.

Full text

Abstract:

A gold nanoparticle-based lateral-flow test strip was developed to detect dimimazene in beef and beef liver. The LOD and cut-off value were evaluated to be 0.1 and 1 μg kg⁻¹ in beef samples, while they 0.1 and 2 μg kg⁻¹ for beef liver samples.

APA, Harvard, Vancouver, ISO, and other styles

45

Chaka, Hassen, and Getachew Abébé. "Trypanosomes résistants aux médicaments : une menace pour la production bovine du sud-ouest éthiopien." Revue d’élevage et de médecine vétérinaire des pays tropicaux 56, no. 1-2 (January 1, 2003): 33. http://dx.doi.org/10.19182/remvt.9872.

Full text

Abstract:

La trypanosomose est une maladie importante du bétail dans le sud-ouest de l’Ethiopie. Actuellement la chimiothérapie et la chimioprévention sont les seules méthodes pratiques de lutte contre la trypanosomose animale mais leur efficacité diminue à cause de l’émergence de chimiorésistances. Parmi les médicaments proposés pour le traitement de la trypanosomose animale, Bérénil® (acéturate de diminazène) et Trypamidium® (chlorure d’isométamidium) sont les plus utilisés du fait de leur disponibilité et de leur toxicité relativement faible pour le bétail. La sensibilité à ces médicaments de quatre souches de Trypanosoma congolense isolées à partir de bovins dans le sud-ouest de l’Ethiopie (Ghibe, Bedelle, Sodo et Arbaminch) a été testée sur des souris blanches (Suisses) et sur des zébus indigènes. Les résultats ont montré que, sur ce nombre limité de souches, des souches de T. congolense étaient résistantes aux médicaments. Les isolats de Ghibe, Bedelle et Sodo se sont révélés résistants aux doses thérapeutiques d’acéturate de diminazène (3,5 mg/kg) ainsi qu’aux doses thérapeutiques et prophylactiques standard de chlorure d’isométamidium (0,5 et 1 mg/kg). Ces trois isolats se sont cependant révélés sensibles à l’acéturate de diminazène à la dose de 7 mg/kg. La souche d’Arbaminch a été résistante aux doses recommandées par les fabricants pour les deux médicaments.

APA, Harvard, Vancouver, ISO, and other styles

46

Ndung’u, Kariuki, Grace Adira Murilla, John Kibuthu Thuita, Geoffrey Njuguna Ngae, Joanna Eseri Auma, Purity Kaari Gitonga, Daniel Kahiga Thungu, Richard Kiptum Kurgat, Judith Kusimba Chemuliti, and Raymond Ellie Mdachi. "Differential virulence of Trypanosoma brucei rhodesiense isolates does not influence the outcome of treatment with anti-trypanosomal drugs in the mouse model." PLOS ONE 15, no. 11 (November 5, 2020): e0229060. http://dx.doi.org/10.1371/journal.pone.0229060.

Full text

Abstract:

We assessed the virulence and anti-trypanosomal drug sensitivity patterns of Trypanosoma brucei rhodesiense (Tbr) isolates in the Kenya Agricultural and Livestock Research Organization-Biotechnology Research Institute (KALRO-BioRI) cryobank. Specifically, the study focused on Tbr clones originally isolated from the western Kenya/eastern Uganda focus of human African Trypanosomiasis (HAT). Twelve (12) Tbr clones were assessed for virulence using groups(n = 10) of Swiss White Mice monitored for 60 days post infection (dpi). Based on survival time, four classes of virulence were identified: (a) very-acute: 0–15, (b) acute: 16–30, (c) sub-acute: 31–45 and (d) chronic: 46–60 dpi. Other virulence biomarkers identified included: pre-patent period (pp), parasitaemia progression, packed cell volume (PCV) and body weight changes. The test Tbr clones together with KALRO-BioRi reference drug-resistant and drug sensitive isolates were then tested for sensitivity to melarsoprol (mel B), pentamidine, diminazene aceturate and suramin, using mice groups (n = 5) treated with single doses of each drug at 24 hours post infection. Our results showed that the clones were distributed among four classes of virulence as follows: 3/12 (very-acute), 3/12 (acute), 2/12 (sub-acute) and 4/12 (chronic) isolates. Differences in survivorship, parasitaemia progression and PCV were significant (P<0.001) and correlated. The isolate considered to be drug resistant at KALRO-BioRI, KETRI 2538, was confirmed to be resistant to melarsoprol, pentamidine and diminazene aceturate but it was not resistant to suramin. A cure rate of at least 80% was achieved for all test isolates with melarsoprol (1mg/Kg and 20 mg/kg), pentamidine (5 and 20 mg/kg), diminazene aceturate (5 mg/kg) and suramin (5 mg/kg) indicating that the isolates were not resistant to any of the drugs despite the differences in virulence. This study provides evidence of variations in virulence of Tbr clones from a single HAT focus and confirms that this variations is not a significant determinant of isolate sensitivity to anti-trypanosomal drugs.

APA, Harvard, Vancouver, ISO, and other styles

47

Echeverria, Jessica Teles, Rodrigo Leite Soares, Beatriz Aléssio Crepaldi, Gustavo Gomes de Oliveira, Polyana Mayume Pereira da Silva, Rayane Chitolina Pupin, Tessie Beck Martins, Herbert Patric Kellermann Cleveland, Carlos Alberto do Nascimento Ramos, and Fernando de Almeida Borges. "Clinical and therapeutic aspects of an outbreak of canine trypanosomiasis." Revista Brasileira de Parasitologia Veterinária 28, no. 2 (April 2019): 320–24. http://dx.doi.org/10.1590/s1984-29612019018.

Full text

Abstract:

Abstract Trypanosomiasis caused by Trypanosoma evansi can seriously affect both domestic and wild animals. This article reports on an outbreak of canine trypanosomiasis on a farm in the Pantanal region of Brazil. The farm had 38 dogs, 20 of which died before receiving veterinary care. The remaining 18 dogs were underwent anamnesisn, clinical examination, hematological and biochemical evaluations. Blood smears and PCR analysis were performed for the diagnosis. The treatment protocols used according to the clinical recovery or parasitological cure of the dogs, using diminazene diaceturate, isometamidium chloride or quinapyramine sulfate. Post-treatment parasitological evaluation was performed by the microhematocrit technique. 7/18 dogs were PCR positive for T. evansi (confirmed by sequencing). There was clinical findings, which were consistent with both the acute and chronic stages of the disease in dogs. The infected dogs all exhibited at least one clinical sign of the disease. The hematological findings were compatible with trypanosomiasis, highlighting the hypochromic microcytic anemia as the main outcome. No treatment protocol was fully effective and the prolonged use of diminazene diaceturate caused the death of an animal. The trypanosomiasis can cause high rates of morbidity and mortality in dogs and difficulty in establishment an effective and safe therapeutic protocol.

APA, Harvard, Vancouver, ISO, and other styles

48

Kwain, Samuel, Gilbert Tetevi, Thomas Mensah, Anil Camas, Mustafa Camas, Aboagye Dofuor, Faustus Azerigyik, Hai Deng, Marcel Jaspars, and Kwaku Kyeremeh. "Digyaindoleacid A: 2-(1-(4-Hydroxyphenyl)-3-oxobut-1-en-2-yloxy)-3-(1H-indol-3-yl)propanoic Acid, a Novel Indole Alkaloid." Molbank 2019, no. 3 (September 14, 2019): M1080. http://dx.doi.org/10.3390/m1080.

Full text

Abstract:

Digyaindoleacid A (1) is one of the novel alkaloids produced by the Ghanaian Paenibacillus sp. DE2SH (GenBank Accession Number: MH091697) isolated from the mangrove rhizosphere soils of the Pterocarpus santalinoides tree growing in the wetlands of the Digya National Park, Brong Ahafo Region, Ghana. This compound was isolated on HPLC at tR ≈ 60 min and its structure determined by MS, 1D, and 2D-NMR data. When tested against Trypanosoma brucei subsp. brucei strain GUTat 3.1, 1 produced a half-maximal inhibitory concentration (IC50) 5.21 μM compared to the standard diminazene aceturate (IC50 = 1.86 μM). In the presence of normal mouse macrophages RAW 264.7, 1 displayed a higher selectivity towards T. brucei subsp. brucei (selectivity indices (SI) = 30.2) with low toxicity. This result is interesting given that the drug diminazene aceturate is considerably toxic and 1 is a natural product isolate. The structure of 1 incorporates the backbone of the amino acid tryptophan which is crucial in the metabolism of Trypanosoma brucei subsp. brucei strain GUTat 3.1. It is possible that 1, could interfere with the normal uptake and metabolism of tryptophan in the parasite. However, 1 (IC50 = 135.41 μM) produced weak antileishmanial activity when tested against Leishmania donovani (Laveran and Mesnil) Ross (D10).

APA, Harvard, Vancouver, ISO, and other styles

49

Peregrine, A. S., M. A. Gray, and S. K. Moloo. "Cross-resistance associated with development of resistance to isometamidium in a clone of Trypanosoma congolense." Antimicrobial Agents and Chemotherapy 41, no. 7 (July 1997): 1604–6. http://dx.doi.org/10.1128/aac.41.7.1604.

Full text

Abstract:

Resistance to isometamidium was increased 94-fold in a clone of Trypanosoma congolense (clone IL 1180) by repeated subcurative treatment of infected mice for 11 months. This was associated with 3.4-, 33-, and 4.2-fold increases in resistance to diminazene, homidium, and quinapyramine, respectively. Both T. congolense IL 1180 and the resistant derivative were able to undergo cyclical development in Glossina morsitans centralis tsetse flies, producing hypopharyngeal infection rates of 40.0 and 39.8%, respectively.

APA, Harvard, Vancouver, ISO, and other styles

50

Tanyıldızı, Sadettin, and Gaffari Türk. "The effects of diminazene aceturate and ceftriaxone on ram sperm." Theriogenology 61, no. 2-3 (January 2004): 529–35. http://dx.doi.org/10.1016/s0093-691x(03)00210-3.

Full text

APA, Harvard, Vancouver, ISO, and other styles

We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!