13146 Abenga, J.N., David, K., Ezebuiro, C.O.G., & Lawani, F.A.G., 2005. Observations on the tolerance of young dogs (puppies) to infection with Trypanosoma congolense. African Journal of Clinical and Experimental Microbiology, 6 (1): 28 - 33.
Abenga: Nigerian Institute for Trypanosomiasis Research, PMB 2077, Kaduna, Nigeria. [[email protected]]
Studies were undertaken to assess the susceptibility of young local dogs to infection with Trypanosoma congolense. Six puppies (7 weeks old) were used for the study. Although the puppies became parasitaemic 6 to 7 days post infection, they were tolerant to infection as the parasitaemia remained low throughout the first seven weeks of the eight-week observation period. The packed cell volume also only dropped slightly during the last four weeks while the mean body weight continued to increase. Similarly, the mean daily body temperature did not differ significantly from those of uninfected control. The significance of trypanotolerance in Nigerian local dogs is discussed.
13147 Abenga, J.N., Enwezor, F.N.C., Lawani, F.A.G., Ezebuiro, C., Sule, J. & David, K.M., 2002. Prevalence of trypanosomosis in trade cattle at slaughter in Kaduna, Nigeria. Nigerian Journal of Parasitology, 23: 107 - 110.
Abenga: Pathology, Epidemiology and Statistics Division, Nigerian Institute for Trypanosomiasis Research, PMB 2077, Kaduna, Kaduna State, Nigeria. [[email protected]]
The prevalence of trypanosomosis in trade cattle at slaughter in Kaduna was investigated during the peak of the rainy season (July to September, 1999). A total of 500 blood samples was collected and parasitologically examined using the haematocrit centrifugation technique and buffy coat method. Physical examination of the animals was done before and after slaughter to assess their clinical condition. The overall infection rate was 3.8 percent. However, 30.9 percent of the animals showed severe emaciation. The infection rate in emaciated animals (7.6 percent) was higher than in non-emaciated animals (2.1 percent). Infected cattle also had significantly lower packed cell volume values than non-infected cattle. The prevalence of trypanosomosis observed in this study does not reflect the true status of the disease in Kaduna State. However, these findings indicate that trypanosomosis has an impact on the physical condition of cattle at slaughter and consequently on the market value.
13148 Abenga, J.N., Enwezor, F.N.C., Lawani, F.A.G., Osue, H.O. & Ikemereh, E.C.D., 2004. Trypanosome prevalence in cattle in Lere area in Kaduna State, North Central Nigeria. Revue d'Élevage et de Médecine vétérinaire des Pays tropicaux, 57 (1 - 2): 45 - 48.
Abenga: Pathology, Epidemiology and Statistics Division, Nigerian Institute for Trypanosomiasis Research, PMB 2077, Kaduna, Kaduna State, Nigeria. [[email protected]]
Trypanosome prevalence in cattle was estimated in August 2001 in selected farms in the three districts of Lere local government area of Kaduna State, North Central Nigeria. The study was subsequent to reports of trypanosomosis outbreaks, which had resulted in deaths of cattle that led to early migration of semi-nomadic Fulanis out of the area, especially during the rains. Blood samples collected randomly from 526 cattle were examined for presence of trypanosomes using the buffy coat technique and Giemsa thin blood smears. Overall, 48 animals were found infected: 39 (81 percent) with Trypanosoma vivax, 7 (15 percent) with T. congolense and 2 (4 percent) with T. brucei. The infection rates in young and adult cattle were 6 and 10 percent, respectively, which were not significantly different. From this study, it is clear that trypanosomosis is still a major obstacle to livestock production in Nigeria and that the incidence rate is similar in young and adult animals.
13149 Cherenet, T., Sani, R.A., Panandam, J.M., Nadzr, S., Speybroeck, N. & van den Bossche, P., 2004. Seasonal prevalence of bovine trypanosomosis in a tsetse-infested zone and a tsetse-free zone of the Amhara Region, north-west Ethiopia. Onderstepoort Journal of Veterinary Research, 71 (4): 307 - 312.
Cherenet: Faculty of Veterinary Medicine, University Putra Malaysia, 43400 Serdang, Malaysia.
During a period of four consecutive years, trypanosomosis surveys were conducted in a tsetse-infested and tsetse-free area of the Amhara Region of north-west Ethiopia. In each study area randomly selected communal cattle were sampled and their blood was investigated using parasitological diagnostic methods. At the same time the population of biting flies was sampled. The monthly average prevalence of trypanosome infections in cattle did not differ significantly between study areas. In both study areas, the prevalence of trypanosome infections was highest during the long rainy season. Trypanosome infections were mainly due to Trypanosoma vivax and they significantly reduced the average packed cell volume and the body condition of the animals. The monthly prevalence of infection was correlated with the density of biting flies, such as Tabanidae and Stomoxys spp., in the preceding month suggesting an important role of mechanical transmission in the epidemiology of trypanosomosis in both areas.
13150 Dinka, H. & Abebe, G., 2005. Small ruminants trypanosomosis in the southwest of Ethiopia. Small Ruminant Research, 57 (2 - 3): 239 - 243.
Abebe: Department of Parasitology, Faculty of Veterinary Medicine, Addis Ababa University, P.O. Box 34, Debre Zeit, Ethiopia.
A study was conducted in two valleys of the southwest Ethiopia (Didessa and Ghibe valleys) from November 2002 to April 2003 to collect baseline data on the prevalence of trypanosomosis in local breeds of sheep and goats. Blood samples from 533 randomly selected small ruminants of different species, sex and age groups were collected and examined with conventional haematological and parasitological techniques. Among the small ruminants examined during the study period 27 animals (5.1 percent) were infected with trypanosomes. Most of the infections were due to Trypanosoma congolense (46.7 percent, 33.3 percent) followed by T. vivax (26.7 percent, 25.0 percent) and the rest was due to T. brucei (6.7 percent, 8.3 percent) and mixed infections of T. congolense and T. vivax (13.3 percent, 25.0 percent), T. brucei and T. vivax (6.7 percent, 8.3 percent) in sheep and goats, respectively. There was no statistically significant difference in infection between male and female, among age groups in sheep and goats as well as valleys. Infection between sheep and goats showed significant difference, the higher being 7.7 percent in sheep and the lower 3.6 percent in goats. Mean packed cell volume (PCV) value of parasitaemic animals was significantly lower than that of aparasitaemic animals. In an attempt to identify the vectors involved in the transmission of small ruminants trypanosomosis, both tsetse flies of the morsitans group (Glossina pallidipes and G. morsitans submorsitans) and palpalis group (G. fuscipes fuscipes) and mechanical vectors of trypanosomosis that belong to Tabanidae (Tabanus) were captured in the lowlands of Didessa (1400 - 1780 m above sea level) and Ghibe (1250 - 1700 m above sea level) valleys. The study revealed that trypanosomosis in sheep and goats is an important disease and small ruminants serve as a potential reservoir of infection for other animals.
13151 Magona, J.W., Walubengo, J. & Olaho-Mukani, W., 2004. Knowledge and attitudes of cattle owners regarding trypanosomosis control in tsetse-infested areas of Uganda. Journal of the South African Veterinary Association, 75 (4): 173 - 176.
Magona: Ministry of Agricultural and Animal Industries & Fisheries, Animal Resources, POBox 105, Entebbe, Uganda.
A pilot survey using a structured questionnaire was conducted in Tororo and Busia districts of Uganda on the knowledge and attitudes of cattle owners regarding tsetse fly and trypanosomosis control, in order to understand factors that hindered their full participation. A total of 81 cattle owners were randomly selected and interviewed, of which 92.5 percent were aware of tsetse flies and trypanosomosis and 87.6 percent recognised animal trypanosomosis as a problem in the area. Most cattle owners were aware of tsetse fly trapping (76.5 percent), isometamidium chloride use (55.5 percent), diminazene aceturate use (48 percent) and pour-on applications (18.5 percent). However, knowledge did not coincide with the application of control measures. Despite the widespread awareness, tsetse fly trapping and pour-on applications were used by only a small percentage of cattle owners (7.5 percent applied tsetse fly trapping while 76.5 percent were aware of it; 1.2 percent applied pour-on insecticides while 18.5 percent were aware of them). Differences between awareness and application were highly significant for tsetse fly trapping and pour-on applications, but not for isometamidium chloride use and diminazene aceturate use. Most cattle owners (97.5 percent) were willing to participate in future control programmes, but preferred participating on a group basis (85.2 percent) rather than individually (14.8 percent). The four most favoured control options in order of importance were: fly traps supplied by the government and maintained by cattle owners; contribution of labour by cattle owners for trap deployment; self-financing of trypanocidal drugs and self-financing of pour-on insecticide. The control options that should be selected in order to elicit full participation by cattle owners are discussed.
13152 Mahama, C.I., Desquesnes, M., Dia, M.L., Losson, B., De Deken, R., Speybroeck, N. & Geerts, S., 2005. A longitudinal epidemiological survey of bovine trypanosomosis and its vectors in the White Volta river basin of Northern Ghana. Veterinary Parasitology, 128 (3 - 4): 201 - 208.
Geerts: Animal Health Department, Institute of Tropical Medicine, Nationalestraat 155, B-2000, Antwerp, Belgium.
A longitudinal epidemiological survey of bovine trypanosomosis and its vectors was carried out in the Volta river basin of Northern Ghana to determine the relationship between cattle management and the incidence of bovine trypanosomosis. Two groups of sentinel cattle under different systems of management, classified as "fully-sedentary" and "partially-sedentary", were followed over a 1-year period starting from March 2003 onwards. Cattle were screened at intervals of three months using the buffy coat technique (BCT). Buffy coat specimen from animals that were positive for the BCT and those that were negative, but with a packed cell volume (PCV) of less than 21 percent, were further tested using the polymerase chain reaction (PCR). Plasma from all animals was tested for antibody using the indirect antibody enzyme-linked immunosorbent assay (ELISA). Trypanosomosis challenge was determined in tandem with the epidemiological survey with watering sites of sentinel cattle being the foci of interest. The parasitological prevalence at the start of the survey was higher in the fully-sedentary group (9 percent) than in the partially-sedentary group (3 percent). In subsequent visits, however, the parasitological incidence was consistently higher in the partially-sedentary group than in the fully-sedentary group. The mean seroprevalence (ELISA) of both groups increased from 3 percent in March to 54 percent in December. Statistical analysis of the serological results using a random effect logistic regression, showed a significant difference in incidence of bovine trypanosomosis between the two groups. There was also a significant effect of time. The influence of cattle herding on host-vector-parasite interface and its consequence on the incidence of trypanosomosis are discussed.
13153 Mochabo, K.O.M., Kitala, P.M., Gathura, P.B., Ogara, W.O., Catley, A., Eregae, E.M. & Kaitho, T.D., 2005. Community perceptions of important camel diseases in Lapur Division of Turkana District, Kenya. Tropical Animal Health and Production, 37 (3): 187 - 204.
Mochabo: Kenya Trypanosomiasis Research Institute (KETRI), PO Box 362, Kikuyu, Kenya.
This paper presents the results of a study conducted in Lapur Division of Turkana District, Kenya, to estimate the incidence and mortality of camel trypanosomosis using participatory methods. Four livestock camps (‘adakars’) were selected for the study. Four informant groups comprising 6 - 8 key persons were used for the participatory exercises. The camel diseases identified by the pastoralists in their order of importance according to annual incidence were: trypanosomosis (11.4 percent); mange (10.8 percent); tick infestation (7.9 percent); haemorrhagic septicaemia (7.7 percent); and non-specific diarrhoea (7.6 percent). Almost half (49.3 percent) of the camel population suffered from at least one disease over the previous year. The annual incidence and mortality rates of trypanosomosis were estimated at 15 percent and 9.9 percent in adult camels and 6.9 percent and 5.2 percent in young camels, respectively. There was a seasonal occurrence of trypanosomosis, with most cases reported in the dry season. The prevalence levels of the disease reportedly declined from about 100 percent in 1978 to an almost stable state of about 15 percent in 2002. This study revealed that camel trypanosomosis is still an important disease in Turkana District, exacting a heavy toll in terms of morbidity and mortality. The economic losses due to the disease were likely to have been great owing to the central role the camel plays in this arid district of Kenya.
13154 Njiru, Z.K., Constantine, C.C., Guya, S., Crowther, J., Kiragu, J.M., Thompson, R.C.A. & Dávila, A.M.R., 2005. The use of ITS1 rDNA PCR in detecting pathogenic African trypanosomes. Parasitology Research, 95 (3): 186 - 192.
Njiru: Division of Veterinary and Biomedical Sciences, Western Australian Biomedical Research Institute (WABRI), Murdoch University, South Street, 6150 Murdoch, Western Australia, Australia.
There are 11 different pathogenic trypanosomes in trypanosomiasis endemic regions of Africa. Their detection and characterisation by molecular methods relies on species-specific primers; consequently several PCR tests have to be made on each sample. Here, new primers have been used and the PCR products assessed for specificity and sensitivity against a range of economically and medically important Trypanosoma species. The primers offer promise as a routine diagnostic tool through the use of a single PCR; however, further evaluation is recommended.
13155 Zinsstag, J. & Schelling, E., 2003. Vector-borne diseases in humans and animals: activities of the Swiss Tropical Institute and risks for Switzerland. SAT, Schweizer Archiv für Tierheilkunde, 145 (12): 559 - 569.
Zinsstag: Swiss Tropical Institute, PO Box, 4002 Basel, Switzerland.
The recent outbreak of anaplasmosis in a Swiss cattle herd triggered a discussion of the risk of vector-borne diseases in animals and humans in relation to climate changes and other factors. This overview presents the Swiss Tropical Institute’s activities on vector-borne diseases (malaria, trypanosomosis, and leishmaniosis in humans and tick-borne diseases in livestock), describes the possible risks for humans and animals in Switzerland, and discusses options for action in the domains of public health, livestock production and companion animals. Switzerland is increasingly confronted with vector-borne diseases in humans and animals, but this is mainly due to an increase in imported cases. The emergence of a disease in one sector (human or veterinary medicine) may predict future trends in the other. A stronger inter-sectoral collaboration between public health and veterinary institutions at the federal and cantonal level is needed.
[See also 28: 13162]
13156 Abenga, J. N., Sanda, S.A., Idowu, T.B. & Lawani F.A.G., 2002. Effect of acute caprine trypanosomiasis on haemoglobin, urea and serum electrolytes. African Journal of Clinical and Experimental Microbiology, 3 (1): 45 - 47.
Abenga: Pathology, Epidemiology and Statistics Division, Nigerian Institute for Trypanosomiasis Research, PMB 2077, Kaduna, Kaduna State, Nigeria. [[email protected]]
The effect of acute caprine trypanosomiasis on haemoglobin concentration, urea and serum electrolytes was studied in Red Sokoto goats infected with Trypanosoma vivax. The course of infection lasted only two weeks when the infected goats died of fulminating parasitaemia and high fever. Haemoglobin concentration of the infected goats was only slightly decreased. However, the serum urea level was significantly increased while Cl, K+, and HCO3 levels were slightly increased above pre-infection values by week two post infection. Serum Na+ increased only in the first week post infection, but returned to pre-infection values by the second week.
13157 Al-Qarawi, A.A., Omar, H.M., Abdel-Rahman, H.A., El-Mougy, S.A. & El-Belely, M.S., 2004. Trypanosomiasis-induced infertility in dromedary (Camelus dromedarius) bulls: changes in plasma steroids concentration and semen characteristics. Animal Reproduction Science, 84: (1 - 2): 73 - 82.
Al-Qarawi: Department of Veterinary Medicine, Faculty of Agriculture and Veterinary Medicine, King Saud University, P.O. Box 1482, Bureidah, Al-Qassim, Saudi Arabia. [[email protected]]
The effect of trypanosomiasis on concentrations of plasma steroids and semen characteristics was studied in 24 dromedary bulls. Based upon the parasitological and serological diagnosis, 18 bulls were found infected with Trypanosoma evansi (Group 2) and six were found to be free from infection and served as controls (Group 1). The infected animals exhibited signs of anaemia indicated by the decrease of packed cell volume (PCV) and haemoglobin concentration (Hb), pale mucus membranes, weight loss, lethargy, weakness and dullness. However, five animals (27.8 percent) of the infected group revealed elevated rectal temperatures and three animals (16.7 percent) revealed testicular degeneration upon palpation of their scrotal contents. Concentrations of plasma oestradiol-17â (86.5 ± 8.6 pg/ml versus 232.5 ± 74.4 pg/ml) and testosterone (4.8 ± 0.7 ng/ml versus 2.7 ± 1.5 ng/ml) were significantly different between the control and infected bulls. The semen collected by electroejaculation was evaluated by a computerised cell motion analyzer; this revealed normal semen characteristics in the control animals compared to sub-normal ones in the infected bulls. There were highly significant decreases in sperm count (12.2 ± 1.3/ml versus 6.5 ± 4.9 × 106 ml-1), motility percentage (68.2 ± 6.7 percent versus 27.4 ± 15.6 percent), percentage of live spermatozoa (73.2 ± 8.3 percent versus 35.8 ± 8.2 percent) and increases in percentage of morphological abnormalities (3.3 ± 0.6 percent versus 15.9 ± 1.0 percent) in the infected group. An examination of the plasma hormonal profiles and semen characteristics in the infected bulls indicated that altered Sertoli cell function due to formation of immune complexes in four bulls (Group 2A), pituitary dysfunction in six bulls (Group 2B), testicular degeneration in three bulls (Group 2C) and finally trypanotolerance in five bulls (Group 2D) are possible factors responsible for poor semen characteristics and infertility induced by T. evansi infection in dromedary bulls.
13158 Darsaud, A., Bourdon, L., Chevrier, C., Keita, M., Bouteille, B., Queyroy, A., Canini, F., Cespuglio, R., Dumas, M. & Buguet, A., 2003. Clinical follow-up in the rat experimental model of African trypanosomiasis. Experimental Biology and Medicine, 228 (11): 1355 - 1362.
Darsaud: Centre de recherches du Service de santé des armées, Département des facteurs humains, La Tronche cedex, France.
Animal models of Human African Trypanosomiasis (HAT) have been developed to understand the pathogenic mechanisms leading to the passage into the neurological phase, most of them referring to histological aspects but not clinical or behavioural data. Our study aimed at defining simple clinical and/or behavioural markers of the passage between the haemolymphatic phase and the meningo-encephalitic stage of the disease. Sprague-Dawley rats (n = 24) were infected with Trypanosoma brucei brucei AnTat 1.1E. Food intake and body weight were measured daily from the day of infection until death. Haematocrit was measured twice a week. Behavioral disturbances were evaluated through an Open-field test. A sudden weight loss occurred on the twelfth day after infection, due to a significant drop of food intake starting two days before. The rats developed an anaemic state shown by the haematocrit measurements. The Open-field test showed them to be less active and reactive as soon as the second week after infestation. A complementary histological study observed trypanosomes and inflammatory cells in the choroid plexus at the same period. These results are in favour of central nervous system functional disturbances. The observed weight loss is discussed as being a measure of the entry in the meningo-encephalitic phase. The rat model reproduces neurological symptoms observed in the human disease and may prove to be useful for further neurohistological and therapeutic studies.
13159 Mbanasor, U.U., Anene, B.M., Chime, A.B., Nnaji, T.O., Eze, J.I. & Ezekwe, A.G., 2003. Haematology of normal and trypanosome-infected Muturu cattle in southeastern Nigeria. Nigerian Journal of Animal Production, 30 (2): 236 - 241.
Mbanasor: Faculty of Veterinary Medicine, University of Nigeria, Nsukka, Nigeria.
Blood parameters of 23 Muturu cattle in a herd were studied between April and August 1998 by monthly examination of their blood samples. Fourteen of a total of 110 blood samples analysed (five samples were unsuitable for analysis) were infected with Trypanosoma vivax. Data from the trypanosome-infected blood were included to evaluate the role of trypanosome infection. The blood values of infected animals were, except for the erythrocyte indices of MCH and MCHC, indistinguishable from those of uninfected animals. There were variations due to age and physiological status (open heifer, pregnant and lactating). Mean RBC and WBC count, MCV and monocyte count were lower in calves than older animals. Open heifers had higher mean RBC and monocyte count, and lower WBC count, MCV and MCH than pregnant and suckling cows.
13160 Shi MeiQing, Wei GuoJian, Pan WanLing & Tabel, H., 2004. Trypanosoma congolense infections: antibody-mediated phagocytosis by Kupffer cells. [mice] Journal of Leukocyte Biology, 76 (2): 399 - 405.
Tabel: Department of Veterinary Microbiology, Western College of Veterinary Medicine, University of Saskatchewan, 52 Campus Drive, Saskatoon, Saskatchewan, S7N 5B4, Canada. [[email protected]]
[See also 28: 13117, 13147]
13161 Agyemang, K., 2005. Trypanotolerant livestock in the context of trypanosomiasis intervention strategies. PAAT Technical and Scientific Series, 7, pp. viii + 66.
Agyemang: International Trypanotolerance Centre, Banjul, Gambia.
An overview is given of the nature of the tsetse-trypanosomiasis problem in Africa, and the various options available for control. The guiding principles are set out for the role of trypanotolerant livestock within an integrated approach to combating the tsetse and trypanosomiasis problem. From this should come a better understanding of where and when trypanotolerant livestock might be used economically and sustainably to combat the tsetse and trypanosomiasis problem. The importance of the attitudes of livestock owners is taken into account.
13162 Faye, D., Fall, A., Leak, S., Losson, B. & Geerts, S., 2005. Influence of an experimental Trypanosoma congolense infection and plane of nutrition on milk production and some biochemical parameters in West African Dwarf goats. Acta Tropica, 93 (3): 247 - 257.
Geerts: Animal Health Department, Institute of Tropical Medicine, Nationalestraat 155, B-2000 Antwerpen, Belgium
The interactions of trypanosomosis and plane of nutrition on health and productivity of multiparous and primiparous West African Dwarf (WAD) does were studied in a multi-factorial experiment including diet (supplementation or basal diet) and infection (infected or control). Experimental does were infected with Trypanosoma congolense at the beginning of the second week post-kidding and monitored for 16 weeks after infection. Trypanosome infection significantly reduced packed cell volume (PCV). Regardless of infection, the drop in PCV from the pre-infection period to the end of the experiment was more severe in animals under restricted diet. Trypanosome parasitaemia tended to be higher in the supplemented group than in the basal diet group and multiparous animals had a higher parasitaemia than primiparous animals. Trypanosome infection as well as dietary supplement had a significant effect on lactation length. Milk off-take from trypanosome-infected does was significantly lower than that from the uninfected control group and there was a positive effect of plane of nutrition. The drop in milk off-take due to trypanosome infection was more severe in the supplemented group than in the group receiving a basal diet due to the number of does from the supplemented group that were withdrawn from the experiment. The effect of trypanosome infection on doe’s live-weight was only noticeable during the first eight weeks of lactation and there was no significant effect on offspring growth rate unless the mother died. Plasma total protein (TP), albumin and cholesterol concentrations were significantly reduced by the infection but were significantly increased by supplementation. Supplemented does had a higher level of cholesterol and a tendency for a higher parasitaemia. Does of high parity also had a higher cholesterol level than primiparous does and, based on the number of animals that were withdrawn from the experiment, they showed a lower resistance to the infection.
13163 Freeman, A.R., Meghen, C.M., MacHugh, D.E., Loftus, R.T., Achukwi, M.D., Bado, A., Sauveroche, B. & Bradley, D.G., 2004. Admixture and diversity in West African cattle populations. Molecular Ecology, 13 (11): 3477 - 3487.
Freeman: Department of Animal Science and Production and Conway Institute of Biomolecular and Biomedical Research, Faculty of Agriculture, University College Dublin, Belfield, Dublin 4, Ireland.
Genetic analysis of microsatellite variation in 16 West African cattle populations was carried out. West Africa represented a unique juxtaposition of different climatic and ecological zones in a relatively small geographical area. While more humid coastal regions were inhabited by the tsetse fly, a vector which spread trypanosomiasis among cattle, the disease was not transmitted in the drier areas outside this zone. This was the most thorough study of genetic diversity in cattle within this area, which contained genetically important trypanotolerant cattle breeds. Genetic relationships among the many breeds were examined and levels of diversity were assessed. Admixture levels were determined using a variety of methods. Ancestry informative or population-associated alleles (PAAs) were selected using populations from India, the Near East and Europe. Multivariate analysis, the admix programme and model-based Bayesian admixture analysis approaches were also employed. These analyses showed the direct impact of ecological factors and the profound effect of admixture on the cattle of this region. Results also highlighted the importance of efforts to prevent further dilution of African taurine breeds by zebu cattle.
13164 Hill, E.W., O’Gorman, G.M., Agaba, M., Gibson, J.P., Hanotte, O., Kemp, S.J., Naessens, J., Coussens, P.M. & MacHugh, D.E., 2005. Understanding bovine trypanosomiasis and trypanotolerance: the promise of functional genomics. Veterinary Immunology and Immunopathology, 105 (3 - 4): 247 - 258.
MacHugh: Animal Genomics Laboratory, Department of Animal Science, Conway Institute for Biomolecular and Biomedical Research, Faculty of Agri-Food and the Environment, University College Dublin, Belfield, Dublin 4, Irish Republic.
African bovine trypanosomiasis, caused by the protozoan parasite Trypanosoma congolense, is endemic throughout sub-Saharan Africa and is a major constraint on livestock production. A promising approach to disease control is to understand and exploit naturally evolved trypanotolerance. We describe the first attempt to investigate the transcriptional response of susceptible Boran (Bos indicus) cattle to trypanosome infection via a functional genomics approach using a bovine total leukocyte cDNA microarray platform. Four male Boran cattle were experimentally infected with T. congolense and peripheral blood mononuclear cells (PBMC) were collected before infection and 13, 17, 23 and 30 days post-infection. A reference experimental design was employed using a universal bovine reference RNA pool. Data were normalised to the median of a set of invariant genes (GAPDH) and BRB-Array tools were used to search for statistically significant differentially expressed genes between each time-point. Using a set of 20 microarray hybridizations, we have made a significant contribution to understanding the temporal transcriptional response of bovine PBMC in vivo to a controlled trypanosome infection. The greatest changes were evident 13 days p.i. after parasites were first detected in the blood. Significant differences were observed in clusters of protein kinase C subunits and MHC class I/II related molecules.
[See also 28: 13135]
13165 Kuboki, N., Sakurai, T., Di Cello, F., Grab, D.J., Suzuki, H., Sugimoto, C. & Igarashi, I., 2003. Loop-mediated isothermal amplification for detection of African trypanosomes. Journal of Clinical Microbiology, 41 (12): 5517 - 5524.
Sakurai: National Research Center for Protozoan Diseases, Obihiro University of Agriculture and Veterinary Medicine, Obihiro, Hokkaido 080-8555, Japan. [[email protected]]
While PCR is a method of choice for the detection of African trypanosomes in both humans and animals, the expense of this method negates its use as a diagnostic method for the detection of endemic trypanosomiasis in African countries. The loop-mediated isothermal amplification (LAMP) reaction is a method that amplifies DNA with high specificity, efficiency, and rapidity under isothermal conditions with only simple incubators. An added advantage of LAMP over PCR-based methods is that DNA amplification can be monitored spectrophotometrically and/or with the naked eye without the use of dyes. Here we report our conditions for a highly sensitive, specific, and easy diagnostic assay based on LAMP technology for the detection of parasites in the Trypanosoma brucei group (including T. brucei brucei, T. brucei gambiense, T. brucei rhodesiense, and T. evansi) and T. congolense. We show that the sensitivity of the LAMP-based method for detection of trypanosomes in vitro is up to 100 times higher than that of PCR-based methods. In vivo studies in mice infected with human-infective T. brucei gambiense further highlight the potential clinical importance of LAMP as a diagnostic tool for the identification of African trypanosomiasis.
13166 Njiru, Z.K., Constantine, C.C., Ndung’u, J.M., Robertson, I., Okaye, S., Thompson, R.C.A. & Reid, S.A., 2004. Detection of Trypanosoma evansi in camels using PCR and CATT/T. evansi tests in Kenya. Veterinary Parasitology, 124 (3 - 4): 187 - 199.
Njiru: Western Australian Biomedical Research Institute, Division of Health Sciences, School of Veterinary and Biomedical Sciences, Murdoch University, South Street, Murdoch, WA 6150, Australia.
[See also 28: 13187]
13167 Abenga, J.N. & Anosa, V.O., 2005. Serum total proteins and creatine levels in experimental Gambian trypanosomosis of vervet monkeys. African Journal of Biotechnology, 4 (2): 187 - 190.
Abenga: Pathology, Epidemiology and Statistics Division, Nigerian Institute for Trypanosomiasis Research, PMB 2077, Kaduna, Kaduna State, Nigeria. [[email protected]]
Although human African trypanosomosis presently constitutes a major socio-economic problem in several parts of sub-Saharan Africa, conflicting reports on experimental infections appear to be one of the factors limiting the chemotherapeutic control of the disease. An attempt was therefore made to evaluate the effect of two strains of Trypanosoma brucei gambiense on total proteins and other serum biochemical parameters using vervet monkeys as a model. The outcome of both strains in vervet monkeys was traumatic as the monkeys died from infection 12 - 15 weeks p.i. while the serum proteins increased due to an increase in the serum globulins with resultant fall in the albumin/globulin ratio. Similarly creatinine and fibrinogen levels increased after infection. The study confirms the existence of atypical virulent infections with a resultant early death from T. b. gambiense.
13168 Darsaud, A., Bourdon, L., Mercier, S., Chapotot, F., Bouteille, B., Cespuglio, R. & Buguet, A., 2004. Twenty-four-hour disruption of the sleep-wake cycle and sleep-onset REM-like episodes in a rat model of African trypanosomiasis. Sleep, 27 (1): 42-46.
Darsaud: Centre de recherches du Service de santé des armées, Département des facteurs humains, B.P. 87, F-38702 La Tronche cedex, France.
Patients with human African trypanosomiasis (sleeping sickness) due to the inoculation of Trypanosoma brucei gambiense or T. b. rhodesiense show a major disruption of the 24-hour sleep-wake distribution, accompanied by the occurrence of sleep-onset rapid-eye-movement (REM) sleep episodes, proportional to the severity of the illness. Although animal models of human African trypanosomiasis have been developed to understand the pathogenic mechanisms leading to immune alterations, the development of an animal model featuring the alterations of endogenous biologic rhythms remains a necessity. Following the description of interventions and experiments on the rat infected with T. b. brucei, it is concluded that the Trypanosoma brucei brucei-infected rat is a good model of the syndrome seen in human African trypanosomiasis, ie the 24-hour disruption of the sleep-wake cycle and the occurrence of sleep-onset REM-like sleep episodes.
13169 Espinoza, E., Sandoval, E., Mavare, M., González, N. & Rangel, L., 2000. Comparación de la serie eritrocítica y leucocítica en ovejas y cabras infectadas con Trypanosoma vivax. [Comparison of erythrocyte and leucocyte changes in sheep and goats infected with Trypanosoma vivax.] Veterinaria Tropical, 25 (1): 29 - 39.
Espinoza: Universidad Simón Rodríguez, Rectorado, Apdo. Postal 3690, Caracas, Venezuela.
13170 Faye, D., Sulon, J., Kane, Y., Beckers, J.F., Leak, S., Kaboret, Y., de Sousa, N.M., Losson, B. & Geerts, S., 2004. Effects of an experimental Trypanosoma congolense infection on the reproductive performance of West African Dwarf goats. Theriogenology, 62 (8): 1438 - 1451.
Geerts: Animal Health Department, Institute of Tropical Medicine, Nationalestraat 155, B-2000, Antwerp, Belgium.
Thirty-six West African Dwarf (WAD) goats were used to assess the effects of an experimental Trypanosoma congolense infection on their reproductive system. Oestrous cycles were synchronised and when confirmed pregnant (n = 31), the does were randomly allocated into control and trypanosome-infected groups. After infection, the animals were carefully observed until parturition. Trypanosome infection caused an increase of rectal temperature, a significant drop in PCV and abortions in 27.8 percent of the infected does. Kids born from infected does had a lower birth weight than kids born from control goats. Eight out of 13 kids (61.5 percent) that were born alive from infected does died during their first week of life. Plasma pregnancy-associated glycoprotein (PAG) and progesterone concentrations were lower in the infected animals than in the controls. In general, PAG concentration in does which aborted dropped before abortion. Our results revealed that artificial T. congolense infection affected reproductive performance of WAD goats with abortions, premature births and perinatal losses being observed. Neither transplacental transmission of T. congolense nor histopathological lesions of the placenta could be demonstrated.
13171 Grab, D.J., Nikolskaia, O., Kim, Y.V., Lonsdale-Eccles, J.D., Ito, S., Hara, T., Fukuma, T., Nyarko, E., Kim, K.J., Stins, M.F., Delannoy, M.J., Rodgers, J. & Kim, K.S., 2004. African trypanosome interactions with an in vitro model of the human blood-brain barrier. Journal of Parasitology, 90 (5): 970 - 979.
Grab: Department of Pediatrics, The Johns Hopkins School of Medicine, Baltimore, MA 21287, USA. [[email protected]]
The neurological manifestations of sleeping sickness in man are attributed to the penetration of the blood-brain barrier (BBB) and invasion of the central nervous system by Trypanosoma brucei gambiense and Trypanosoma brucei rhodesiense. However, how African trypanosomes cross the BBB remains an unresolved issue. We have examined the traversal of African trypanosomes across the human BBB using an in vitro BBB model system constructed of human brain microvascular endothelial cells (BMECs) grown on Costar Transwell inserts. Human-infective T. b. gambiense strain IL 1852 was found to cross human BMECs far more readily than the animal-infective T. b. brucei strains 427 and TREU 927. Tsetse fly-infective procyclic trypomastigotes did not cross the human BMECs either alone or when coincubated with the bloodstream form T. b. gambiense. After overnight incubation, the integrity of the human BMEC monolayer measured by transendothelial electrical resistance was maintained on the inserts relative to the controls when the endothelial cells were incubated with T. b. brucei. However, decreases in electrical resistance were observed when the BMEC-coated inserts were incubated with T. b. gambiense. Light and electron microscopy studies revealed that T. b. gambiense initially bind at or near intercellular junctions before crossing the BBB paracellularly. This is the first demonstration of paracellular traversal of African trypanosomes across the BBB. Further studies are required to determine the mechanism of BBB traversal by these parasites at the cellular and molecular level.
13172 Mgbenka, B.O. & Ufele, A.N., 2004. Effects of dietary supplementation of vitamin E and selenium on blood parameters of trypanosome-infected rats (Rattus rattus). Bio-research, 2 (1): 8 - 17.
Mgbenka: Department of Zoology, University of Nigeria, Nsukka, Nigeria.
This study was carried out to evaluate the combined effects of dietary supplementation of vitamin E and selenium on total white blood cells, mononucleated cells, polymorphonucleated cells and packed cell volume of Trypanosoma congolense-infected rats (Rattus rattus). Ninety adult R. rattus were used. The rats were randomly assigned to 6 treatment groups (A - F). Each treatment was replicated three times. The rats were fed chicks’ mash-based diets containing varied quantities of vitamin E and selenium. In treatment A, the control, neither vitamin E nor selenium was included in the diet, and in other treatments (B - F) the chicks’ mash contained different levels of vitamin E and selenium: diet B, 0.1 mg selenium and 60 mg of vitamin E; diet C, 0.3 mg selenium and 80 mg vitamin E; diet D, 0.5 mg selenium and 100 mg vitamin E; diet E, 0.3 mg selenium and 0.0 mg vitamin E; and diet F, 0.0 mg selenium and 80 mg vitamin E. Blood samples of the rats from each treatment were taken on a weekly basis. The experiment lasted five weeks and at the end of which it was found that 0.3 mg selenium and 80 mg vitamin E (diet C) significantly enhanced the resistance of the R. rattus against trypanosomiasis; the rats lived beyond the usual 10 - 20 days after being infected with T. congolense.
13173 Naessens, J., Kitani, H., Nakamura, Y., Yagi, Y., Sekikawa, K. & Iraqi, F., 2005. TNF-á mediates the development of anaemia in a murine Trypanosoma brucei rhodesiense infection, but not the anaemia associated with a murine Trypanosoma congolense infection. Clinical and Experimental Immunology, 139 (3): 405 - 410.
Iraqi: International Livestock Research Institute, PO Box 30709, 00100 Nairobi, Kenya.
Development of anaemia in inflammatory diseases is cytokine-mediated. Specifically, the levels of tumour necrosis factor-á (TNF-á), produced by activated macrophages, are correlated with severity of disease and anaemia in infections and chronic disease. In African trypanosomiasis, anaemia develops very early in infection around the time when parasites become detectable in the blood. Since the anaemia persists after the first waves of parasitaemia when low numbers of trypanosomes are circulating in the blood, it is generally assumed that anaemia is not directly induced by a parasite factor, but might be cytokine-mediated, as in other cases of anaemia accompanying inflammation. To clarify the role of TNF-á in the development of anaemia, blood parameters of wild type (TNF-á+/+), TNF-á-null (TNF-á-/-) and TNF-á-hemizygous (TNF-á-/+) trypanotolerant mice were compared during infections with the cattle parasite Trypanosoma congolense. No differences in PCV, erythrocyte numbers or haemoglobin were observed between TNF-á-deficient and wild type mice, suggesting that the decrease in erythrocytes was not mediated by TNF-á. Erythropoetin (EPO) levels increased during infection and no significant differences in EPO levels were observed between the three mouse strains. In contrast, during an infection with the human pathogen Trypanosoma brucei rhodesiense, the number of red blood cells in TNF-á-deficient mice remained significantly higher than in the wild type mice. These data suggest that more than one mechanism promotes the development of anaemia associated with trypanosomiasis.
13174 Campbell, M., Prankerd, R.J., Davie, A.S. & Charman, W.N., 2004. Degradation of berenil (diminazene aceturate) in acidic aqueous solution. Journal of Pharmacy and Pharmacology, 56 (10): 1327 - 1332.
Campbell: Centre for Drug Candidate Optimisation, Victorian College of Pharmacy, Monash University (Parkville Campus), 381 Royal Parade, Parkville, Victoria 3052, Australia.
The trypanocide berenil was assessed for chemical stability over the pH range 1 - 8 at 37°C and 0.2 M ionic strength. It was found to be sufficiently unstable under acid conditions that its therapeutic efficacy is most likely severely compromised when administered orally. At pH 3, the half-life was 35 min, decreasing to 1.5 min at pH 1.75. Reaction rate constants were corrected for the effects of buffer catalysis and were found to range from 2.00 min-1 at pH 1 to 6.1 × 10-6 min-1 at pH 8. The pH-rate profile displayed a region (pH 1 - 4) where specific acid catalysis was dominant, followed by a transitional region (pH 5 - 7), and finally a region (pH>7) where uncatalysed degradation was most important. It is recommended that berenil be enteric coated for formulations to be used in treating Third World parasitic diseases.
13175 Dembitsky, V.M. & Levitsky, D.O., 2004. Arsenolipids. Progress in Lipid Research, 43 (5): 403 - 448.
Dembitsky: Department of Organic Chemistry, P.O. Box 39231, Hebrew University, Jerusalem 91391, Israel.
Natural arsenolipids are analogues of neutral lipids, like monoglycerides, glycolipids, phospho- and also phosphonolipids. They have been found in microorganisms, fungi, plants, lichens, in marine molluscs, sponges, other invertebrates, and in fish tissues. This review presents structures of natural arsenolipids (and derivatives), their distribution, biogenesis in algae and invertebrates, synthesis, and also biological activity. Arsenolipids are thought to be end products of arsenate detoxification processes, involving reduction and oxidative methylation and adenosylation. The proposed biogenesis of arsenolipids is based on the natural occurrence of arsenic metabolites, and all the intermediates in the proposed pathway have been identified as natural products of algal origin. Different arseno species are shown to be inhibitors of glycerol kinase, bovine carbonic anhydrase, and also are an effective therapy for acute promyelocytic leukaemia, and there has been promising activity noted in other haematologic and solid tumours. Arsonoliposomes demonstrated high anti-trypanosomal activity against Trypanosoma brucei and inhibit growth of some types of cancer cells (HL-60, C6 and GH3).
13176 Fujii, N., Mallari, J.P., Hansell, E.J., Mackey, Z., Doyle, P., Zhou, Y.M., Gut, J., Rosenthal, P.J., McKerrow, J.H. & Guy, R.K., 2005. Discovery of potent thiosemicarbazone inhibitors of rhodesain and cruzain. Bioorganic & Medicinal Chemistry Letters, 15 (1): 121 - 123.
Guy: Department of Pharmaceutical Chemistry, University of California, San Francisco, CA 94143, USA.
The synthesis and evaluation of a series of thiosemicarbazones as potential inhibitors of cysteine proteases relevant to parasitic diseases are reported. Derivatives of thiosemicarbazone 1 were discovered to be potent inhibitors of cruzain and rhodesain, crucial proteases in the life cycles of Trypanosoma cruzi and T. brucei rhodesiense, the organisms causing Chagas’ disease and sleeping sickness. However, the entire series had only modest potency against falcipain-2, an essential protease for Plasmodium falciparum, the organism causing malaria. Among the active inhibitors, several potently inhibited proliferation of cultures of T. brucei. However, only modest activity was observed in inhibition of proliferation of T. cruzi or P. falciparum.
13177 Huysmans, G., Ranquin, A., Wyns, L., Steyaert, J. & Gelder, P. van, 2005. Encapsulation of therapeutic nucleoside hydrolase in functionalised nanocapsules. Journal of Controlled Release, 102 (1): 171 - 179.
van Gelder: Department of Molecular and Cellular Interactions, Flanders Interuniversity Institute for Biotechnology (VIB), Free University Brussels, Pleinlaan 2, 1050 Brussels, Belgium.
Liposomes are introduced as encapsulating carriers for prodrug activating enzymes. The technique used is described in detail. The authors state that with these vesicles they have introduced a new strategy for prodrug therapy.
13178 Joubert, K.E., Kettner, F., Lobetti, R.G. & Miller, D.M., 2003. The effects of diminazene aceturate on systemic blood pressure in clinically healthy adult dogs. Journal of the South African Veterinary Association, 74 (3): 69 - 71.
Joubert: Department of Companion Animal Clinical Studies, Faculty of Veterinary Science, University of Pretoria, Private Bag X04, Onderstepoort, 0110, South Africa.
Diminazene aceturate is a commonly used antibabesial agent. It has been postulated that diminazene may induce a decrease in blood pressure and exacerbate the hypotension presented in dogs with babesiosis. This study was undertaken to assess the effect of diminazene aceturate on the blood pressure of healthy dogs. Six healthy German shepherd dogs between 18 and 24 months of age with a mean weight of 30.4±2.75 kg were used. Blood pressure was directly measured at the following time intervals: -5, 0, 5, 10, 15, 20, 25, 30, 35, 40, 50, 60, 90 and 120 minutes after treatment with diminazene aceturate (4.2 mg/kg) intramuscularly. No statistical difference (P>0.05) was found in blood pressure between any of the time intervals. An increase in heart rate was seen 5 minutes after the administration of diminazene aceturate but no change in blood pressure was evident. This study concluded that diminazene aceturate in its current formulation with antipyrine does not alter blood pressure in healthy adult dogs.
13179 Khabnadideh, S., Pez, D., Musso, A., Brun, R., Pérez, L.M.R., Gonzalez-Pacanowska, D. & Gilbert, I.H., 2005. Design, synthesis and evaluation of 2,4-diaminoquinazolines as inhibitors of trypanosomal and leishmanial dihydrofolate reductase. Bioorganic and Medicinal Chemistry, 13 (7): 2637 - 2649.
Gilbert: Welsh School of Pharmacy, Cardiff University, Redwood Building, King Edward VII Avenue, Cardiff, CF10 3XF, UK.
This paper describes the design, synthesis and evaluation of a series of 2,4-diaminoquinazolines as inhibitors of leishmanial and trypanosomal dihydrofolate reductase. Compounds were designed by generating a virtual library of compounds and docking them into the enzyme active site. Following their synthesis, they were found to be potent and selective inhibitors of leishmanial dihydrofolate reductase. The compounds were also found to have potent activity against Trypanosoma brucei rhodesiense, a causative organism of African trypanosomiasis and also against T. cruzi, the causative organism of Chagas’disease. There was significantly lower activity against Leishmania donovani, one of the causative organisms of leishmaniasis.
13180 Machocho, A.K., Bastida, J., Codina, C., Viladomat, F., Brun, R. & Chhabra, S.C., 2004. Augustamine type alkaloids from Crinum kirkii. Phytochemistry, 65 (23): 3143 - 3149.
Chhabra: Department of Chemistry, Kenyatta University, PO Box 43844, 00100 GPO, Nairobi, Kenya.
Sixteen more Amaryllidaceae alkaloids have been isolated from bulbs of Crinum kirkii of which noraugustamine and 4a,N-dedihydronoraugustamine are hitherto unknown. Their structures and those of earlier known alkaloids have been established by physical and spectroscopic analysis. Application of 2D NMR techniques was used for complete characterization of the alkaloids as well as of 3-O-acetylsanguinine. 1,2-diacetyllycorine and 3-O-acetylsanguinine showed activity against Trypanosoma brucei rhodesiense, the parasite associated with sleeping sickness. 3-O-acetylsanguinine also showed some activity against Trypanosoma cruzi.
13181 Magona, J.W., Mayende, J.S.P., Okiria, R. & Okuna, N.M., 2004. Protective efficacy of isometamidium chloride and diminazene aceturate against natural Trypanosoma brucei, Trypanosoma congolense and Trypanosoma vivax infections in cattle under a suppressed tsetse population in Uganda. Onderstepoort Journal of Veterinary Research, 71 (3): 231 - 237.
Magona: Livestock Health Research Institute, P.O. Box 96, Tororo, Uganda.
The protective efficacy of isometamidium chloride (ISMM) and diminazene aceturate (DIM) against Trypanosoma brucei, Trypanosoma congolense and Trypanosoma vivax infections in cattle under a suppressed tsetse population was assessed in southeast Uganda. A total of 66 and 57 trypanosome-infected cattle were treated with ISMM and DIM respectively, together with 177 trypanosome-free animals not treated, and were followed for 12 months, checking every 4 weeks. There was no statistical difference in the mean time to infection with any trypanosome species in animals treated with ISMM or DIM. However, the mean time to trypanosome infection was significantly longer for treated animals than controls. The mean time to infection with each of the three trypanosome species differed significantly, with the average time to T. vivax infection the lowest, followed by T. congolense and then T. brucei. The protective efficacy of DIM was as good as that of ISMM, implying that curative treatments against trypanosomosis are sufficient for combination with tsetse control. These results indicate that isometamidium chloride and diminazene aceturate have retained their effectiveness against trypanosome infections in southeast Uganda, despite their use over many years.
13182 Mbwambo, Z.H., Apers, S., Moshi, M.J., Kapingu, M.C., Van Miert, S., Claeys, M., Brun, R., Cos, P., Pieters, L. & Vlietinck, A., 2004. Anthranoid compounds with antiprotozoal activity from Vismia orientalis. [T. b. rhodesiense] Planta Medica, 70 (8): 706 - 710.
Mbwambo: Institute of Traditional Medicine, Muhimbili University College of Health Sciences, Dar es Salaam, Tanzania.
A phytochemical investigation of the 80 percent ethanolic extract of stem bark of Vismia orientalis (Guttiferae or Clusiaceae), a plant used in traditional medicine in Tanzania, resulted in the isolation and spectroscopic characterisation of several compounds, of which vismione D exhibited a broad range of antiprotozoal activities including some against Trypanosoma brucei rhodesiense. However, the compound was also slightly cytotoxic against human L6 cells.
13183 Molfetta, F.A., Bruni, A.T., Honorio, K.M. & da Silva, A.B.F., 2005. A structure-activity relationship study of quinine compounds with trypanocidal activity. European Journal of Medicinal Chemistry, 40 (4): 329 - 338.
da Silva: Departamento de Química e Física Molecular, Instituto de Química de São Carlos, Universidade de São Paulo, CP 780, 13560-970 São Carlos, SP, Brazil.
13184 Moyersoen, J., Choe, J.-W., Fan, E.K., Hol, W.G.J. & Michels, P.A.M., 2004. Biogenesis of peroxisomes and glycosomes: trypanosomatid glycosome assembly is a promising new drug target. FEMS Microbiology Reviews, 28 (5): 603 - 643.
Michels: Research Unit for Tropical Diseases, Christian de Duve Institute of Cellular Pathology and Laboratory of Biochemistry, Université Catholique de Louvain, ICP-TROP 74.39, Avenue Hippocrate 74, B-1200 Brussels, Belgium. [[email protected]]
In trypanosomatids (Trypanosoma and Leishmania), protozoa responsible for serious diseases of mankind in tropical and subtropical countries, core carbohydrate metabolism including glycolysis is compartmentalised in peculiar peroxisomes called glycosomes. Proper biogenesis of these organelles and the correct sequestering of glycolytic enzymes are essential to these parasites. Biogenesis of glycosomes in trypanosomatids and that of peroxisomes in other eukaryotes, including the human host, occur via homologous processes involving proteins called peroxins, which exert their function through multiple, transient interactions with each other. Decreased expression of peroxins leads to death of trypanosomes. Peroxins show only a low level of sequence conservation. Therefore, it seems feasible to design compounds that will prevent interactions of proteins involved in biogenesis of trypanosomatid glycosomes without interfering with peroxisome formation in the human host cells. Such compounds would be suitable as lead drugs against diseases caused by trypanosomatids.
13185 Nishimura, K., Shima, K., Asakura, M., Ohnishi, Y. & Yamasaki, S., 2005. Effects of heparin administration on Trypanosoma brucei gambiense infection in rats. Journal of Parasitology, 91 (1): 219 - 222.
Nishimura: Division of Veterinary Science, Graduate School of Agriculture and Biological Sciences, Osaka Prefecture University, 1-1, Gakuencho, Sakai, Osaka 599-8531, Japan. [[email protected]]
We examined whether heparin administration influences in vivo trypanosome proliferation in infected rats. Administration of heparin every 8 hours via cardiac catheter inhibited growth of Trypanosoma brucei gambiense and prolonged survival of treated rats. Heparin administration increased lipoprotein lipase activity, high-density lipoprotein (HDL) concentration in the blood, and haptoglobin messenger RNA content of the liver. The presence of heparin in culture media did not directly affect proliferation of trypanosomes in vitro. However, the addition of plasma from infected rats treated with heparin to culture media decreased the number of trypanosomes. This effect was decreased by incubating the trypanosomes with benzyl alcohol, a known inhibitor of receptor-mediated endocytosis of lipoprotein. These data suggested that heparin administration reduced the number of trypanosomes in infected rats. Trypanosome lytic factor, a HDL and haptoglobin-related protein, protects humans and some animals from infection by Trypanosoma brucei brucei. In rats, increases in HDL and haptoglobin may affect the proliferation of T. b. gambiense.
13186 Nyasse, B., Ngantchou, I., Tchana, E.M., Sonké, B., Denier, C. & Fontaine, C., 2004. Inhibition of both Trypanosoma brucei bloodstream form and related glycolytic enzymes by a new kolavic acid derivative isolated from Entada abyssinica. Pharmazie, 59 (11): 873 - 875.
Nyasse: Laboratory of Bio-organic and Medicinal Chemistry, Department of Organic Chemistry, Faculty of Science, University of Yaounde I, Box 812 Yaounde, Cameroon.
13187 Othman, O.E. & Ahmed, S., 2004. Cytogenetic effect of the trypanocidal drug berenil in blood cultures of river buffalo. Journal of Biological Sciences, 4 (2): 180 - 184.
Othman: Department of Cell Biology, National Research Center, Dokki, Giza, Cairo, Egypt.
The cytogenetic effect of berenil was evaluated at three concentrations (0.25, 0.5, and 1 mg ml-1) on river buffalo lymphocyte cultures in vitro. The formation of chromosomal aberrations, the induction of sister chromatid exchanges, and the measurement of micronuclei formation were the cytogenetic parameters used in the study. The results showed that the number of cells with different types of structural chromosomal aberrations, including breaks, gaps, deletions, fragments and centric fusions, were increased significantly with the three doses of berenil as compared with the control. It is concluded that the three cytogenetic parameters used to evaluate the effect of diminazine aceturate (berenil) indicate that this drug has a mutagenic effect on river buffalo lymphocyte cultures.
13188 Salem, M.M. & Werbovetz, K.A., 2005. Antiprotozoal compounds from Psorothamnus polydenius. Journal of Natural Products, 68 (1): 108 - 111.
Werbovetz: Division of Medicinal Chemistry and Pharmacognosy, College of Pharmacy, The Ohio State University, Columbus, OH 43210, USA.
Fractionation of the methanolic extract of Psorothamnus polydenius led to the identification of a number of compounds, which were tested in vitro for their antiprotozoal activity against Leishmania donovani and Trypanosoma brucei. Chalcones 1 and 2 and dalrubone exhibited leishmanicidal and trypanocidal properties.
13189 Seebacher, W., Schlapper, C., Brun, R., Kaiser, M., Saf, R. & Weis, R., 2005. Antiprotozoal activities of new bicyclo[2.2.2]octan-2-imines and esters of bicyclo[2.2.2]octan-2-ols. European Journal of Pharmaceutical Sciences, 24 (4): 281 - 289.
Seebacher: Institute of Pharmaceutical Sciences, Pharmaceutical Chemistry, Karl-Franzens University, Universitätsplatz 1, A-8010 Graz, Austria.
13190 Silva Filho, A.A. da, Albuquerque, S., e Silva, M.L.A., Eberlin, M.N., Tomazela, D.M. & Bastos, J.K., 2004. Tetrahydrofuran lignans from Nectandra megapotamica with trypanocidal activity. Journal of Natural Products, 67 (1): 42 - 45.
Eberlin: Faculdade de Ciências Farmacêuticas de Ribeirão Preto, Universidade de São Paulo, Avenida do Café S/N, Ribeirão Preto, 14040-903, SP, Brazil.
13191 Steverding, D. & Scory, S., 2004. Trypanosoma brucei: unexpected azide sensitivity of bloodstream forms. Journal of Parasitology, 90 (5): 1188 - 1190.
Steverding: School of Biological Sciences, University of Bristol, Woodland Road, Bristol BS8 1UG, UK. [[email protected]]
Bloodstream forms of Trypanosoma brucei lack cytochromes and are, therefore, insensitive to cyanide. Azide is a toxic anion that bears chemical and biological properties in common with cyanide and may act in a similar way by inhibition of cytochrome c oxidase. It was, therefore, surprising to find that bloodstream forms of T. brucei were sensitive to sodium azide; growth was reduced by 50 percent with 0.1 mM sodium azide. So far, the only enzyme known in bloodstream forms of T. brucei to be sensitive to azide is the iron-containing superoxide dismutase. However, because the activity of the superoxide dismutase was not affected in parasites incubated for 16 h with 0.5 mM sodium azide (a concentration at which no cell proliferates), the toxic action of azide cannot be due to inhibition of this enzyme. These results indicate that the general toxicity of azide is different from that of cyanide.
13192 Tanyildizi, S. & Türk, G., 2004. The effects of diminazene aceturate and ceftriaxone on ram sperm. Theriogenology, 61 (2 - 3): 529 - 535.
Tanyildizi: Department of Pharmacology and Toxicology, Faculty of Veterinary Medicine, Firat University, 23119 Elazið, Turkey.
Effects of diminazene aceturate and ceftriaxone disodium were evaluated on sperm quality of rams. Daily intramuscular injections of diminazene (6 mg/kg) or ceftriaxone (28.5 mg/kg) were given to each of seven Akkaraman rams assigned per drug for two days. Semen samples were collected from the rams at post-treatment 1, 4, 24, 48, 72, 144, 288 and 336 h and examined for sperm characteristics and hyaluronidase activity. Results showed that use of ceftriaxone and diminazene caused significant (P<0.01) decreases in sperm concentration, volume and motility compared to control group within 288 h post-treatment. In addition, hyaluronidase activity increased significantly (P<0.01) in semen of rams treated with ceftriaxone while remained unchanged in those received diminazene. In conclusion, diminazene aceturate and ceftriaxone disodium did not have any deleterious effect on hyaluronidase enzyme. However, both drugs caused impairment of sperm in rams during the 288 h.
13193 Tasdemir, D., Brun, R., Perozzo, R. & Donmez, A.A., 2005. Evaluation of antiprotozoal and plasmodial enoyl-ACP reductase inhibition potential of Turkish medicinal plants. Phytotherapy Research, 19 (2): 162 - 166.
Tasdemir: Institute of Organic Chemistry, University of Zurich, Winter-thurerstrasse 190, CH-8057 Zürich, Switzerland. [[email protected]]
A total of 58 extracts of different polarity were prepared from various organs of 16 species of Turkish plants and screened for their antitrypanosomal, antileishmanial and antiplasmodial activities. No significant activity was observed against Trypanosoma cruzi, whereas many extracts showed appreciable trypanocidal potential against T. brucei rhodesiense, with the CHCl3-soluble portion of Phlomis kurdica being the most active.
13194 Tasdemir, D., Güner, N.D., Perozzo, R., Brun, R., Dönmez, A.A., Calis, I. & Rüedi, P., 2005. Anti-protozoal and plasmodial FabI enzyme inhibiting metabolites of Scrophularia lepidota roots. Phytochemistry, 66 (3): 355 - 362.
Tasdemir: Institute of Organic Chemistry, University of Zurich, Winter-thurerstrasse 190, CH-8057 Zürich, Switzerland.
13195 Tsujimura, Y., Watarai, S., Uemura, A., Ohnishi, Y. & Kodama, H., 2005. Effect of anti-ganglioside antibody in experimental Trypanosoma brucei infection in mice. Research in Veterinary Science, 78 (3): 245 - 247.
Wataraia: Laboratory of Veterinary Immunology, Division of Veterinary Science, Graduate School of Agriculture and Biological Sciences, Osaka Prefecture University, 1-1 Gakuen-cho, Sakai, Osaka 599-8531, Japan.
The effect of antibody against ganglioside antigen on Trypanosoma brucei parasites was examined in vitro and in vivo using anti-ganglioside GM1 (AGM-1) monoclonal antibody. The antibody showed complement-dependent cytotoxicity against T. brucei with mouse complement. Furthermore, mice given AGM-1 were challenged intraperitoneally with T. brucei. Although all non-treated control mice died within six days after infection, all of AGM-1-injected mice had survived by six days post-infection. These data suggest that antibody against ganglioside antigen on T. brucei has potential in protection against T. brucei infection.
13196 Uemura, A., Watarai, S., Ohnishi, Y. & Kodama, H., 2005. Protective effect of antiganglioside antibodies against experimental Trypanosoma brucei infection in mice. Journal of Parasitology, 91 (1): 73 - 78.
Watarai: Laboratory of Veterinary Immunology, Division of Veterinary Science, Graduate School of Agriculture and Biological Sciences, Osaka Prefecture University, Sakai, Osaka 599-8531, Japan. [[email protected]]
Liposome-associated ganglioside antigens (ganglioside GM1 or bovine brain gangliosides) were prepared to evaluate the potential protective efficacy against Trypanosoma brucei. Mice were immunized with liposome-associated ganglioside GM1 or bovine brain gangliosides intraperitoneally (i.p.). After immunization, significantly higher antigen-specific IgG and IgM antibodies were detected in sera than in the non-immunized control group. When sera from immunized mice were analyzed for isotype distribution, antigen-specific IgG1, IgG2a, and IgG3 antibody responses were also noted. After immunization, mice were challenged i.p. with 1 × 102 cells of T. brucei. Sixty percent of liposome-associated ganglioside GM1-immunized mice survived the infection, and all the mice immunized with bovine brain gangliosides-containing liposomes survived. However, all control mice died within seven days after infection. These data demonstrate that liposomes containing ganglioside antigens have the potential usefulness for the induction of a protective immune response against T. brucei infection and suggest the possibility of developing vaccines that may ultimately be used for the prevention of trypanosomiasis.
13197 Verlinde, C.L.M.J., Bressi, J.C., Choe, J., Suresh, S., Buckner, F.S., Van Voorhis, W.C., Michels, P.A.M., Gelb, M.H. & Hol, W.G.J., 2002. Protein structure-based design of anti-protozoal drugs. [T. brucei] Journal of the Brazilian Chemical Society, 13 (6): 843 - 848.
Verlinde: Biomolecular Structure Center, University of Washington, Box 357742, Seattle, WA98195-7742, USA. [[email protected]]
The repertoire of drugs to fight protozoal diseases such as malaria, Chagas’ disease, leishmaniasis and African trypanosomiasis is woefully inadequate. Now, genome sequencing and structural genomics projects are quickly elucidating new drug targets, providing incredible opportunities for medicinal chemists. Here, we illustrate the power of structure-based drug design in this process by our efforts to selectively block trypanosomal glycolysis.
13198 Wesongah, J.O., Murilla, G.A., Kibugu, J.K. & Jones, T.W., 2004. Evaluation of isometamidium levels in the serum of sheep and goats after prophylactic treatment against trypanosomosis. Onderstepoort Journal of Veterinary Research, 71 (3): 175 - 179.
Wesongah: Kenya Trypanosomiasis Research Institute, P.O. Box 362, Kikuyu, Kenya.
Isometamidium chloride has been used for the control of trypanosomosis in animals for over 36 years, but recently there have been reports of prophylaxis failure under natural conditions. In this study, use of the drug for prophylactic purpose against trypanosomosis in small ruminants was investigated. Forty-two sheep and 44 goats were divided into four treatment groups. Groups 1 and 2 were treated with isometamidium chloride (Samorin) at 3-month intervals while groups 3 and 4 were used as controls. All the animals were exposed to natural tsetse challenge and monitored for serum isometamidium levels and anti-trypanosome antibodies. Seven days after drug administration, isometamidium levels were significantly higher in goats 13.7 ± 0.07 ng/ml than in sheep 6.2 ± 0.06 ng/ml. However, the elimination half-life in the sheep was 14.2 ± 0.92 days and was significantly higher than that of the goats 12 ± 0.5 days. This study established that isometamidium metabolism differs between sheep and goats and this difference may have important implications in high tsetse challenge areas.
13199 Witola, W.H., Inoue, N., Ohashi, K. & Onuma, M., 2004. RNA-interference silencing of the adenosine transporter-1 gene in Trypanosoma evansi confers resistance to diminazene aceturate. Experimental Parasitology, 107 (1 - 2): 47 - 57.
Onuma: Graduate School of Veterinary Medicine, Hokkaido University, Sapporo 060-0818, Japan. [[email protected]]
Drug resistance of trypanosomes is now a problem, but its underlying mechanisms are not fully understood. Cellular uptake of the major trypanocidal drugs is thought to occur through an adenosine transporter. The adenosine transporter-1 gene, TbAT1, encoding a P2-like nucleoside transporter has previously been cloned from Trypanosoma brucei brucei, and when expressed in yeast, it showed very similar substrate specificity to the P2-nucleoside transporter, but could not transport diamidines (pentamidine and diminazene). We have cloned and sequenced a similar gene (TevAT1) from Trypanosoma evansi and found it to have 99.7 percent identity to the TbAT1 gene. To elucidate the role of the TevAT1 gene on diamidine trypanocidal effect, we genetically engineered T. evansi for conditional knock-out of the TevAT1 gene by RNA interference (RNAi). Induction of the RNAi resulted in 10-fold depletion of TevAT1 mRNA, with concomitantly significant resistance to diminazene aceturate (berenil). The induced parasites propagated normally and attained peak cell density at an in vitro concentration of berenil, 5.5-fold higher than the IC100 of the wild-type. TevAT1 knock-out had no effect on the trypanocidal activity of suramin and antrycide, but conferred some resistance to samorin. Our findings validate the significance of the TevAT1 adenosine transporter-1 gene in mediating the trypanocidal effect of diamidines in T. evansi. Further, we show for the first time that RNAi gene silencing in T. evansi can be induced using plasmids designed for T. brucei. We also demonstrate the usefulness of real-time PCR in rapidly quantifying mRNA levels in trypanosomes.
[See also 28: 13283]
[See also 28: 13124, 13125]
13200 Ackers, J.P., Dhir, V. & Field, M.C., 2005. A bioinformatic analysis of the RAB genes of Trypanosoma brucei. Molecular and Biochemical Parasitology, 141 (1): 89 - 97.
Field: Wellcome Trust Laboratories for Molecular Parasitology, Department of Biological Sciences, Imperial College, Exhibition Road, London SW7 2AY, UK. [[email protected]]
13201 Alibu, V.P., Storm, L., Haile, S., Clayton, C. & Horn, D., 2004. A doubly inducible system for RNA interference and rapid RNAi plasmid construction in Trypanosoma brucei. Molecular and Biochemical Parasitology, 139 (1): 75 - 82.
Clayton: Zentrum für Molekulare Biologie der Universität Heidelberg, ZMBH, Im Neuenheimer Feld 282, D-69120 Heidelberg, Germany.
13202 Allen, J.W.A., Ginger, M.L. & Ferguson, S.J., 2004. Maturation of the unusual single-cysteine (XXXCH) mitochondrial c-type cytochromes found in trypanosomatids must occur through a novel biogenesis pathway. Biochemical Journal, 383 (3): 537 - 542.
Allen: Department of Biochemistry, University of Oxford, South Parks Road, Oxford, OX1 3QU, UK. [[email protected]]
13203 Allen, J.W.A., Ginger, M.L. & Ferguson, S.J., 2005. Complexity and diversity in c-type cytochrome biogenesis systems. Biochemical Society Transactions, 33 (1): 145 - 146.
Allen: Department of Biochemistry, University of Oxford, South Parks Road, Oxford, OX1 3QU, UK. [[email protected]]
13204 Alsford, S., Glover, L. & Horn, D., 2004. Multiplex analysis of RNA interference defects in Trypanosoma brucei. Molecular and Biochemical Parasitology, 139 (1): 129 - 132.
Horn: London School of Hygiene and Tropical Medicine, Keppel Street, London WC1E 7HT, UK.
13205 Ansede, J.H., Anbazhagan, M., Brun, R., Easterbrook, J.D., Hall, J.E. & Boykin, D.W., 2004. O-alkoxyamidine prodrugs of furamidine: in vitro transport and microsomal metabolism as indicators of in vivo efficacy in a mouse model of Trypanosoma brucei rhodesiense infection. Journal of Medicinal Chemistry, 47 (17): 4335 - 4338.
Ansede: Division of Drug Delivery and Disposition, School of Pharmacy, The University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599-7360, USA.
13206 Baticados, W.N., Witola, W.H., Inoue, N., Kim, J.Y., Kuboki, N., Xuan, X.N., Yokoyama, N. & Sugimoto, C., 2005. Expression of a gene encoding Trypanosoma congolense putative abc1 family protein is developmentally regulated. Journal of Veterinary Medical Science, 67 (2): 157 - 164.
Inoue: National Research Centre for Protozoan Diseases, Obihiro University of Agriculture and Veterinary Medicine, Hokkaido 0808555, Japan.
13207 Becker, M., Aitcheson, N., Byles, E., Wickstead, B., Louis, E. & Rudenko, G., 2004. Isolation of the repertoire of VSG expression site containing telomeres of Trypanosoma brucei 427 using transformation-associated recombination in yeast. Genome Research, 14 (11): 2319 - 2329.
Rudenko: Peter Medawar Building for Pathogen Research, University of Oxford, Oxford OX1 5SY, UK. [[email protected]]
13208 Berriman, M., 2004. The genomes of eukaryotic pathogens. South African Journal of Science, 100 (9 - 10): 452 - 458.
Berriman: The Wellcome Trust Sanger Institute, Genome Campus, Hinxton, CB10 1SA, UK.
13209 Best, A., Handoko, L., Schlüter, E. & Göringer, H.U., 2005. In vitro synthesised small interfering RNAs elicit RNA interference in African trypanosomes. Journal of Biological Chemistry, 280 (21): 20573 - 20579.
Göringer: Dept. of Microbiology and Genetics, Darmstadt University of Technology, Schnittspahnstrasse 64287 Darmstadt, Germany. [goringer@ hrzpub.tu-darmstadt.de]
13210 Besteiro, S., Barrett, M.P., Rivière, L. & Bringaud, F., 2005. Energy generation in insect stages of Trypanosoma brucei: metabolism in flux. Trends in Parasitology, 21 (4): 185 - 191.
Bringaud: Laboratoire de Génomique Fonctionnelle des Trypanosomatides, UMR-5162 CNRS, Université Victor Segalen Bordeaux 2, Bordeaux, France.
The generation of energy in African trypanosomes is a subject of undoubted importance. In bloodstream-form organisms, substrate-level phosphorylation of glucose is sufficient to provide the energy needs of the parasite. The situation in procyclic-form trypanosomes is more complex. For many years, it was accepted that glucose metabolism followed a conventional scheme involving glycolysis, the tricarboxylic acid cycle and ATP-producing oxidative phosphorylation linked to the electron-transport chain. However, progress in sequencing the Trypanosoma brucei genome and the development of gene-knockout and RNA interference technology has provided novel insights. Coupling these new technologies with classical approaches, including NMR and mass spectrometry to analyse glycolytic intermediates and end products, has yielded several surprises. In this article, we summarise how these recent data have helped to change the view of metabolism in procyclic-form T. brucei.
13211 Brems, S., Guilbride, D.L., Gundlesdodjir-Planck, D., Busold, C., Luu, V.-D., Schanne, M., Hoheisel, J. & Clayton, C., 2004. The transcriptomes of Trypanosoma brucei Lister 427 and TREU927 bloodstream and procyclic trypomastigotes. Molecular and Biochemical Parasitology, 139 (2): 163 - 172.
Clayton: DKFZ, Im Neuenheimer Feld 580, D 69120 Heidelberg, Germany.
13212 Camargo, R.E., Uzcanga, G.L. & Bubis, J., 2004. Isolation of two antigens from Trypanosoma evansi that are partially responsible for its cross-reactivity with Trypanosoma vivax. Veterinary Parasitology, 123 (1 - 2): 67 - 81.
Bubis: Laboratorio de Química de Proteínas, Departamento de Biología Celular, División de Ciencias Biológicas, Universidad Simón Bolívar, Apartado 89.000, Valle de Sartenejas, Baruta, Caracas 1081-A, Venezuela.
13213 Charrière, F., Tan, T.H.P. & Schneider, A., 2005. Mitochondrial initiation factor 2 of Trypanosoma brucei binds imported formylated elongator-type tRNAMet. Journal of Biological Chemistry, 280 (16): 15659 - 15665.
Schneider: From the Department of Biology/Zoology, University of Fribourg, Chemin du Musée 10, CH-1700 Fribourg, Switzerland. [[email protected]]
13214 Chattopadhyay, A., Jones, N.G., Nietlispach, D., Nielsen, P.R., Voorheis, H.P., Mott, H.R. & Carrington, M., 2005. Structure of the C-terminal domain from Trypanosoma brucei variant surface glycoprotein MITat1.2. Journal of Biological Chemistry, 280 (8): 7228 - 7235.
Carrington: Department of Biochemistry, University of Cambridge, 80 Tennis Court Road, Cambridge CB2 1GA, UK. [[email protected]]
13215 Chowdhury, S.F., Guerrero, R.H., Brun, R., Ruiz-Perez, L.M., Pacanowska, D.G. and Gilbert, I.H., 2002. Synthesis and testing of 5-benzyl-2,4-diaminopyrimidines as potential inhibitors of leishmanial and trypanosomal dihydrofolate reductase. [T. brucei] Journal of Enzyme Inhibition and Medicinal Chemistry, 17 (5): 293 - 302.
Gilbert: Welsh School of Pharmacy, Cardiff University, Redwood Building, King Edward VII Avenue, Cardiff, CF 10 3XF, UK.
13216 Chung Wei-Lien, Carrington, M. & Field, M.C., 2004. Cytoplasmic targeting signals in transmembrane invariant surface glycoproteins of trypanosomes. Journal of Biological Chemistry, 279 (52): 54887 - 54895.
Field: Department of Pathology, Tennis Court Road, University of Cambridge, Cambridge CB2 1QP, UK. [[email protected]]
13217 Dacks, J.B. & Doolittle, W.F., 2004. Molecular and phylogenetic characterization of syntaxin genes from parasitic protozoa. Molecular and Biochemical Parasitology, 136 (2): 123 - 136.
Dacks: Department of Zoology, The Natural History Museum, Cromwell Road, London SW7 5BD, UK.
13218 Dardonville, C., Rinaldi, E., Barrett, M.P., Brun, R., Gilbert, I.H. & Hanau, S., 2004. Selective inhibition of Trypanosoma brucei 6-phosphogluconate dehydrogenase by high-energy intermediate and transition-state analogues. Journal of Medicinal Chemistry, 47 (13): 3427 - 3437.
Gilbert: Welsh School of Pharmacy, Redwood Building, Cardiff University, King Edward VII Avenue, Cardiff CF10 3XF, U.K.
13219 Deng, J.P., Schnaufer, A., Salavati, R., Stuart, K.D. & Hol, W.G.J., 2004. High resolution crystal structure of a key editosome enzyme from Trypanosoma brucei: RNA editing ligase 1. Journal of Molecular Biology, 343 (3): 601 - 613.
Hol: Howard Hughes Medical Institute, University of Washington, Seattle, WA 98195, USA. [[email protected]]
13220 Dhir, V., Allen, C.L. & Field, M.C., 2005. Perturbation of local endogenous expression by insertion of Pol I expression constructs into the genome of Trypanosoma brucei. Experimental Parasitology, 109 (3): 198 - 200.
Field: Department of Biological Sciences, Imperial College, London SW7 2AY, UK. [[email protected]]
13221 Dhir, V., Goulding, D. & Field, M.C., 2004. TbRAB1 and TbRAB2 mediate trafficking through the early secretory pathway of Trypanosoma brucei. Molecular and Biochemical Parasitology, 137 (2): 253 - 265.
Field: Department of Biological Sciences, Imperial College, London, SW7 2AY, UK. [[email protected]]
13222 DiPaolo, C., Kieft, R., Cross, M. & Sabatini, R., 2005. Regulation of trypanosome DNA glycosylation by a SWI2/SNF2-like protein. Molecular Cell, 17 (3): 441 - 451.
Sabatini: Global Infectious Diseases Program, Marine Biological Laboratory, Woods Hole, MA 02543 USA. [[email protected]]
13223 Downey, N., Hines, J.C., Sinha, K.M. & Ray, D.S., 2005. Mitochondrial DNA ligases of Trypanosoma brucei. Eukaryotic Cell, 4 (4): 765-774.
Ray: Paul D. Boyer Hall, 611 Charles Young Dr., University of California, Los Angeles, CA 90095-1570 USA. [[email protected]]
13224 Durand-Dubief, M. & Bastin, P., 2003. TbAGO1, an Argonaute protein required for RNA interference, is involved in mitosis and chromosome segregation in Trypanosoma brucei. BMC Biology, 1 (2): pp. (12 December 2003). [see http://www.biomedcentral.com/1741-7007/1/2]
Bastin: INSERM U565 & CNRS UMR8646, MNHN USM0503, Muséum National d'Histoire Naturelle, 43 rue Cuvier, 75231 Paris cedex 05, France.
13225 Field, M.C., Allen, C.L., Dhir, V., Goulding, D., Hall, B.S., Morgan, G.W., Veazey, P. & Engstler, M., 2004. New approaches to the microscopic imaging of Trypanosoma brucei. Microscopy and Microanalysis, 10 (5): 621 - 636.
Field: Department of Biological Sciences, Imperial College, London, SW7 2AY, UK. [[email protected]]
Protozoan parasites are fearsome pathogens responsible for a substantial proportion of human mortality, morbidity, and economic hardship. The principal disease agents are members of the orders Apicomplexa (Plasmodium, Toxoplasma, Eimeria) and Kinetoplastida (trypanosomes, Leishmania). The majority of humans are at risk from infection from one or more of these organisms, with profound effects on the economy, social structure and quality of life in endemic areas; Plasmodium itself accounts for over one million deaths per annum, and an estimated 4 × 107 disability-adjusted life years (DALYs), whereas the Kinetoplastida are responsible for over 100,000 deaths per annum and 4 × 106 DALYs. Current control strategies are failing due to drug resistance and inadequate implementation of existing public health strategies. Trypanosoma brucei, the African trypanosome, has emerged as a favoured model system for the study of basic cell biology in Kinetoplastida, because of several recent technical advances (transfection, inducible expression systems, and RNA interference), and these advantages, together with genome sequencing efforts, are widely anticipated to provide new strategies of therapeutic intervention. Here we describe a suite of methods that have been developed for the microscopic analysis of T. brucei at the light and ultrastructural levels, an essential component of analysis of gene function and hence identification of therapeutic targets.
13226 Figarella, K., Rawer, M., Uzcategui, N.L., Kubata, B.K., Lauber, K., Madeo, F., Wesselborg, S. & Duszenko, M., 2005. Prostaglandin D-2 induces programmed cell death in Trypanosoma brucei bloodstream form. Cell Death and Differentiation, 12 (4): 335 - 346.
Duszenko: Department of Chemistry and Pharmacy, Interfakultäres Institut für Biochemie, University of Tübingen, Hoppe-Seyler-Str. 4, Tübingen, Germany. [[email protected]]
13227 Gadelha, C., Wickstead, B., Souza, W. de, Gull, K. & Cunha-e-Silva, N., 2005. Cryptic paraflagellar rod in endosymbiont-containing kinetoplastid protozoa. Eukaryotic Cell, 4 (3): 516 - 525.
Gadelha: Sir William Dunn School of Pathology, University of Oxford, South Parks Road, Oxford OX1 3RE, UK. [catarina.gadelha@path. ox.ac.uk]
13228 Gao, G.H., Simpson, A.M., Kang, X.D., Rogers, K., Nebohacova, M., Li, F. & Simpson, L., 2005. Functional complementation of Trypanosoma brucei RNA in vitro editing with recombinant RNA ligase. Proceedings of the National Academy of Sciences of the United States of America, 102 (13): 4712 - 4717.
Simpson: Howard Hughes Medical Institute, University of California, 6780 MRL, 675 Charles E. Young Drive South, Los Angeles, CA 90095, USA. [[email protected]]
13229 Glenn, R.J., Pemberton, A.J., Royle, H.J., Spackman, R.W., Smith, E., Rivett, A.J. & Steverding, D., 2004. Trypanocidal effect of alpha´, beta´-epoxyketones indicates that trypanosomes are particularly sensitive to inhibitors of proteasome trypsin-like activity. International Journal of Antimicrobial Agents, 24 (3): 286 - 289.
Steverding: School of Biological Sciences, University of Bristol, Woodland Road, Bristol BS8 1UG, UK. [[email protected]]
13230 Greenbaum, D.C., Mackey, Z., Hansell, E., Doyle, P., Gut, J., Caffrey, C.R., Lehrman, J., Rosenthal, P.J. & McKerrow, J.H. & Chibale, K., 2004. Synthesis and structure-activity relationships of parasiticidal thiosemi-carbazone cysteine protease inhibitors against Plasmodium falciparum, Trypanosoma brucei, and Trypanosoma cruzi. Journal of Medicinal Chemistry, 47 (12): 3212 - 3219.
Greenbaum: Sandler Center for Basic Research in Parasitic Diseases, Department of Pathology, University of California, San Francisco, California 94143, USA.
13231 Guerreiro, L.T.A., Souza, S.S., Wagner, G., De Souza, E.A., Mendes, P.N., Campos, L.M., Barros, L., Pires, P.F., Campos, M.L.M., Grisard, E.C. & Dávila, A.M.R., 2005. Exploring the genome of Trypanosoma vivax through GSS and in silico comparative analysis. Omics, 9 (1): 116 - 128.
Dávila: Departamento de Bioquímica e Biologia Molecular, Instituto Oswaldo Cruz/Fundação Oswaldo Cruz, Rio de Janeiro, Brazil.
13232 Hall, B., Allen, C.L., Goulding, D. & Field, M.C., 2004. Both of the Rab5 subfamily small GTPases of Trypanosoma brucei are essential and required for endocytosis. Molecular and Biochemical Parasitology, 138 (1): 67 - 77.
Field: Department of Biological Sciences, Imperial College, Exhibition Road, London SW7 2AY, UK. [[email protected]]
13233 Hall, B.S., Arun Pal, Goulding, D. & Field, M.C., 2004. Rab4 is an essential regulator of lysosomal trafficking in trypanosomes. Journal of Biological Chemistry, 279 (43): 45047 - 45056.
Field: Department of Biological Sciences, Imperial College, London SW7 2AY, UK. [[email protected]]
13234 Hall, B.S., Smith, E., Langer, W., Jacobs, L.A., Goulding, D. & Field, M.C., 2005. Developmental variation in Rab11-dependent trafficking in Trypanosoma brucei. Eukaryotic Cell, 4 (5): 971 - 980.
Field: Department of Pathology, Tennis Court Road, University of Cambridge, Cambridge CB2 1QP, UK. [[email protected]]
13235 Hammarton, T.C., Lillico, S.G., Welburn, S.C. & Mottram, J.C., 2005. Trypanosoma brucei MOB1 is required for accurate and efficient cytokinesis but not for exit from mitosis. Molecular Microbiology, 56 (1): 104 - 116.
Mottram: Wellcome Centre for Molecular Parasitology, The Anderson College, University of Glasgow, 56 Dumbarton Road, Glasgow G11 6NU, UK. [[email protected]]
13236 Inoue, M., Nakamura, Y., Yasuda, K., Yasaka, N., Hara, T., Schnaufer, A., Stuart, K. & Fukuma, T., 2005. The 14-3-3 proteins of Trypanosoma brucei function in motility, cytokinesis, and cell cycle. Journal of Biological Chemistry, 280 (14): 14085 - 14096.
Inoue: Department of Parasitology, Kurume University School of Medicine, 67 Asahi-machi, Kurume, Fukuoka 830-0011, Japan.
13237 Janzen, C.J., Lander, F., Dreesen, O. & Cross, G.A.M., 2004. Telomere length regulation and transcriptional silencing in KU80-deficient Trypanosoma brucei. Nucleic Acids Research, 32 (22): 6575 - 6584.
Cross: Laboratory of Molecular Parasitology, The Rockefeller University, Box 185, 1230 York Avenue, New York, NY 10021-6399, USA. [[email protected]]
13238 Jones, D., Mehlert, A. & Ferguson, M.A.J., 2004. The N-glycan glucosidase system in Trypanosoma brucei. Biochemical Society Transactions, 32 (5): 766 - 768.
Jones: School of Life Sciences, University of Dundee, Dundee DD1 5EH, UK. [[email protected]]
13239 Kang, X.D., Rogers, K., Gao, G.H., Falick, A.M., Zhou, S. & Simpson, L., 2005. Reconstitution of uridine-deletion precleaved RNA editing with two recombinant enzymes. [Trypanosomatid mitochondria] Proceedings of the National Academy of Sciences of the United States of America, 102 (4): 1017 - 1022.
Simpson: Howard Hughes Medical Institute, University of California, Los Angeles, CA 90095, USA. [[email protected]]
13240 Kao, C.Y. & Read, L.K., 2005. Opposing effects of polyadenylation on the stability of edited and unedited mitochondrial RNAs in Trypanosoma brucei. Molecular and Cellular Biology, 25 (5): 1634 - 1644.
Read: Department of Microbiology and Immunology and Witebsky Center for Microbial Pathogenesis and Immunology, SUNY Buffalo School of Medicine, Buffalo, New York, USA.
13241 Kessler, P.S. & Parsons, M., 2005. Probing the role of compartmentation of glycolysis in procyclic form Trypanosoma brucei: RNA interference studies of PEX14, hexokinase, and phosphofructokinase. Journal of Biological Chemistry, 280 (10): 9030 - 9036.
Parsons: Seattle Biomedical Research Institute, Seattle, Washington 98109, USA. [[email protected]]
13242 Kita, K., Nihei, C. & Tomitsuka, E., 2003. Parasite mitochondria as drug target: diversity and dynamic changes during the life cycle. Current Medicinal Chemistry, 10 (23): 2535 - 2548.
Department of Biomedical Chemistry, Graduate School of Medicine, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-0033, Japan.
13243 Lanteri, C.A., Trumpower, B.L., Tidwell, R.R. & Meshnick, S.R., 2004. DB75, a novel trypanocidal agent, disrupts mitochondrial function in Saccharomyces cerevisiae. Antimicrobial Agents and Chemotherapy, 48 (10): 3968 - 3974.
Tidwell: Department of Pathology and Laboratory Medicine, Room 805, Brinkhous-Bullitt Building, University of North Carolina, Chapel Hill, NC 27599-7525, USA. [Tidwell@ med.unc.edu]
13244 Law, J.A., Huang, C.E., O’Hearn, S.F. & Sollner-Webb, B., 2005. In Trypanosoma brucei RNA editing, band II enables recognition specifically at each step of the U insertion cycle. Molecular and Cellular Biology, 25 (7): 2785 - 2794.
Sollner-Webb: Department of Biological Chemistry, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA. [bsw@ jhmi.edu].
13245 Laxman, S., Rascón, A. & Beavo, J.A., 2005. Trypanosome cyclic nucleotide phosphodiesterase 2B binds cAMP through its GAF-A domain. Journal of Biological Chemistry, 280 (5): 3771 - 3779.
Beavo: Department of Pharmacology, University of Washington, Seattle, Washington 98195-7280, USA. [[email protected]]
13246 Lecordier, L., Walgraffe, D., Devaux, S., Poelvoorde, P., Pays, E. & Vanhamme, L., 2005. Trypanosoma brucei RNA interference in the mammalian host. [Mice] Molecular and Biochemical Parasitology, 140 (1): 127 - 131.
Vanhamme: Laboratory of Molecular Parasitology, Institute for Molecular Biology and Medicine (IBMM), Free University of Brussels, 12 rue des Professeurs Jeener et Brachet, 6041 Gosselies, Belgium. [zknjiru@ hotmail.com]
13247 Lewdorowicz, M., Yoffe, Y., Zuberek, J., Jemielity, J., Stepinski, J., Kierzek, R., Stolarski, R., Shapira, M. & Darzynkiewicz, E., 2004. Chemical synthesis and binding activity of the trypanosomatid cap-4 structure. RNA, 10 (9): 1469 - 1478.
Darzynkiewicz: Department of Biophysics, Institute of Experimental Physics, Warsaw University, 93 Zwirki and Wigury St., 02-089 Warsaw, Poland [[email protected]]
13248 Liang, X.H., Uliel, S., Hury, A., Barth, S., Doniger, T., Unger, R. & Michaeli, S., 2005. A genome-wide analysis of C/D and H/ACA-like small nucleolar RNAs in Trypanosoma brucei reveals a trypanosome-specific pattern of rRNA modification. RNA, 11 (5): 619 - 645.
Michaeli: Faculty of Life Sciences, Bar-Ilan University, Ramat-Gan 52900, Israel. [[email protected]]
13249 Liniger, M., Urwyler, S., Studer, E., Oberle, M., Renggli, C. K. & Roditi, I., 2004. Role of the N-terminal domains of EP and GPEET procyclins in membrane targeting and the establishment of midgut infections by Trypanosoma brucei. Molecular and Biochemical Parasitology, 137 (2): 247 - 251.
Roditi: Institut für Zellbiologie, Universität Bern, Baltzerstrasse 4, CH-3012 Bern, Switzerland.
13250 Lowell, J.E. & Cross, G.A.M., 2004. A variant histone H3 is enriched at telomeres in Trypanosoma brucei. Journal of Cell Science, 117 (24): 5937 - 5947.
Cross: Laboratory of Molecular Parasitology, The Rockefeller University, 1230 York Avenue, New York, NY 10021, USA. [george.cross@ rockefeller.edu]
13251 Mackey, Z.B., O’Brien, T.C., Greenbaum, D.C., Blank, R.B. & McKerrow, J.H., 2004. A cathepsin B-like protease is required for host protein degradation in Trypanosoma brucei. Journal of Biological Chemistry, 279 (46): 48426 - 48433.
Mackey: Department of Pathology Tropical Disease Research Unit, University of California, 513 Parnassus HSW 501, San Francisco, CA 94143, USA. [[email protected]]
13252 Mao, J., Gao, Y.G., Odeh, S., Robinson, H., Montalvetti, A., Docampo, R. & Oldfield, E., 2004. Crystallization and preliminary X-ray diffraction study of the farnesyl diphosphate synthase from Trypanosoma brucei. Acta Crystallographica Section D, Biological Crystallography, 60 (10): 1863 - 1866.
Oldfield: Department of Chemistry and Biophysics, University of Illinois at Urbana-Champaign, 600 South Matthews Avenue, Urbana, IL 61801, USA. [[email protected]]
13253 Matthews, K.R., 2005. The developmental cell biology of Trypanosoma brucei. Journal of Cell Science, 118 (2): 283 - 290.
Matthews: Institute of Immunology and Infection Research, School of Biological Sciences, University of Edinburgh, West Mains Road, Edinburgh, EH9 3JT, UK. [[email protected]]
Trypanosoma brucei provides an excellent system for studies of many aspects of cell biology, including cell structure and morphology, organelle positioning, cell division and protein trafficking. However, the trypanosome has a complex life cycle in which it must adapt either to the mammalian bloodstream or to different compartments within the tsetse fly. These differentiation events require stage-specific changes to basic cell biological processes and reflect responses to environmental stimuli and programmed differentiation events that must occur within a single cell. The organization of cell structure is fundamental to the trypanosome throughout its life cycle. Modulations of the overall cell morphology and positioning of the specialised mitochondrial genome, flagellum and associated basal body provide the classical descriptions of the different life cycle stages of the parasite. The dependency relationships that govern these morphological changes are now beginning to be understood and their molecular basis identified. The overall picture emerging is of a highly organized cell in which the rules established for cell division and morphogenesis in organisms such as yeast and mammalian cells do not necessarily apply. Therefore, understanding the developmental cell biology of the African trypanosome is providing insight into both fundamentally conserved and fundamentally different aspects of the organization of the eukaryotic cell.
13254 Morgan, G.W., Denny, P.W., Vaughan, S., Goulding, D., Jeffries, T.R., Smith, D.F., Gull, K. & Field, M.C., 2005. An evolutionarily conserved coiled-coil protein implicated in polycystic kidney disease is involved in basal body duplication and flagellar biogenesis in Trypanosoma brucei. Molecular and Cellular Biology, 25 (9): 3774 - 3783.
Field: Department of Pathology, Tennis Court Road, University of Cambridge, Cambridge CB2 1QP, UK. [[email protected]]
13255 Morty, R.E., Shih, A.Y., Fülöp, V. & Andrews, N.W., 2005. Identification of the reactive cysteine residues in oligopeptidase B from Trypanosoma brucei. FEBS Letters, 579 (10): 2191 - 2196.
Morty: Department of Internal Medicine, University of Giessen School of Medicine, Aulweg 123 (Room 6-11), D-35392 Giessen, Germany
13256 Mussmann, R., Engstler, M., Gerrits, H., Kieft, R., Toaldo, C.B., Onderwater, J., Koerten, H., van Luenen, H.G.A.M. & Borst, P., 2004. Factors affecting the level and localization of the transferrin receptor in Trypanosoma brucei. Journal of Biological Chemistry, 279 (39): 40690 - 40698.
Borst: The Netherlands Cancer Institute, Division of Molecular Biology, Plesmanlaan 121, 1066 CX Amsterdam, Netherlands. [[email protected]]
13257 Natto, M.J., Wallace, L.J.M., Candlish, D., Al-Salabi, M.I., Coutts, S.E. & de Koning, H.P., 2005. Trypanosoma brucei: expression of multiple purine transporters prevents the development of allopurinol resistance. Experimental Parasitology, 109 (2): 80 - 86.
de Koning: Division of Infection and Immunity, Institute of Biomedical and Life Sciences, University of Glasgow, Joseph Black Building, Glasgow G12 8QQ, UK.
13258 Nilsson, D. & Andersson, B., 2005. Strand asymmetry patterns in trypanosomatid parasites. Experimental Parasitology, 109 (3): 143 - 149.
Andersson: Centre for Genomics and Bioinformatics, Karolinska Institutet, Berzeliusv. 35, SE-171 77 Stockholm, Sweden
13259 Nyame, A.K., Kawar, Z.S. & Cummings, R.D., 2004. Antigenic glycans in parasitic infections: implications for vaccines and diagnostics. Archives of Biochemistry and Biophysics, 426 (2): 182 - 200.
Cummings: Department of Biochemistry and Molecular Biology, Oklahoma Center for Medical Glycobiology, University of Oklahoma Health Sciences Center, Biomedical Research Center, Room 417, 975 NE 10th Street, Oklahoma City, OK 73104, USA. [[email protected]]
13260 Palfi, Z., Schimanski, B., Günzl, A., Lücke, S. & Bindereif, A., 2005. U1 small nuclear RNP from Trypanosoma brucei: a minimal U1 snRNA with unusual protein components. Nucleic Acids Research, 33 (8): 2493 - 2503.
Bindereif: Institut für Biochemie, Justus-Liebig-Universität Giessen Heinrich-Buff-Ring 58, D-35392 Giessen, Germany [albrecht.bindereif@ chemie.bio.uni-giessen.de]
13261 Papageorgiou, I.G., Yakob, L., Al Salabi, M.I., Diallinas, G., Soteriadou, K.P. & De Koning, H.P., 2005. Identification of the first pyrimidine nucleobase transporter in Leishmania: similarities with the Trypanosoma brucei U1 transporter and antileishmanial activity of uracil analogues. Parasitology, 130 (3): 275 - 283.
De Koning: Institute of Biomedical and Life Sciences, Division of Infection and Immunity, University of Glasgow, Glasgow G12 8QQ, UK.
13262 Peacock, L., Bailey, M. & Gibson, W., 2005. Tetracycline induction of gene expression in Trypanosoma brucei within the tsetse fly vector. Molecular and Biochemical Parasitology, 140 (2): 247 - 249.
Gibson: School of Biological Sciences, University of Bristol, Woodland Road, Bristol BS8 1UG, UK.
13263 Price, H.P., Panethymitaki, C., Goulding, D. & Smith, D.F., 2005. Functional analysis of TbARL1, an N-myristoylated Golgi protein essential for viability in bloodstream trypanosomes. Journal of Cell Science, 118 (4): 831 - 841.
Smith: Wellcome Trust Laboratories for Molecular Parasitology, Centre for Molecular Microbiology and Infection, Department of Biological Sciences, Imperial College London, London, SW7 2AZ, UK. [[email protected]]
13264 Raes, G., Brys, L., Dahal, B.K., Brandt, J., Grooten, J., Brombacher, F., Vanham, G., Noël, W., Bogaert, P., Boonefaes, T., Kindt, A., Bergh, R. van den, Leenen, P.J.M., Baetselier, P. de & Ghassabeh, G.H., 2005. Macrophage galactose-type C-type lectins as novel markers for alternatively activated macrophages elicited by parasitic infections and allergic airway inflammation. [T. b. brucei] Journal of Leukocyte Biology, 77 (3): 321 - 327.
Raes: Cellular and Molecular Immunology Unit, Vlaams Interuniversitair Instituut voor Biotechnologie, Vrije Universiteit Brussel, Building E, Level 8, Pleinlaan 2, B-1050 Brussels, Belgium.
13265 Rivière, L., van Weelden, S.W.H., Glass, P., Vegh, P., Coustou, V., Biran, M., van Hellemond, J.J., Bringaud, F., Tielens, A.G.M. & Boshart, M., 2004. Acetyl:succinate CoA-transferase in procyclic Trypanosoma brucei: gene identification and role in carbohydrate metabolism. Journal of Biological Chemistry, 279 (44): 45337 - 45346.
Boshart: Laboratoire de Genomique Fonctionnelle des Trypanosomatides, UMR-5162 CNRS, Université Victor Segalen Bordeaux II, 33076 Bordeaux Cedex, France. [[email protected]]
13266 Roper, J.R., Guther, M.L.S., MacRae, J.I., Prescott, A.R., Hallyburton, I., Acosta-Serrano, A. & Ferguson, M.A.J., 2005. The suppression of galactose metabolism in procylic form Trypanosoma brucei causes cessation of cell growth and alters procyclin glycoprotein structure and copy number. Journal of Biological Chemistry, 280 (20): 19728 - 19736.
Ferguson: Department of Pathology, University of Cambridge, Tennis Court Road, Cambridge CB2 1QP, UK. [[email protected]]
13267 Rusconi, F., Durand-Dubief, M. & Bastin, P., 2005. Functional complementation of RNA interference mutants in trypanosomes. BMC Biotechnology, 5 - art. no. 6.
Bastin: UMR5153 CNRS, USM0503 MNHN, U565 INSERM 57, rue Cuvier B.P. 26, F-75231, Paris Cedex 05, France.
13268 Ryan, C.M. & Read, L.K., 2005. UTP-dependent turnover of Trypanosoma brucei mitochondrial mRNA requires UTP polymerization and involves the RET1 TUTase. RNA, 11 (5): 763 - 773.
Read: Department of Microbiology and Witebsky Center for Microbial Pathogenesis and Immunology, School of Medicine and Biomedical Sciences, State University of New York at Buffalo, Buffalo, NY 14214, USA. [[email protected]]
13269 Sahin, A., Lemercier, G., Tetaud, E., Espiau, B., Myler, P., Stuart, K., Bakalara, N. & Merlin, G., 2004. Trypanosomatid flagellum biogenesis: ARL-3A is involved in several species. Experimental Parasitology, 108 (3 - 4): 126 - 133.
Merlin: Laboratoire de Génomique Fonctionnelle des Trypanosomatides, UMR CNRS 5162, Université de Bordeaux 2, 146 Rue Léo Saignat, 33 000 Bordeaux, France.
13270 Salmon, D., Paturiaux-Hanocq, F., Poelvoorde, P., Vanhamme, L. & Pays, E., 2005. Trypanosoma brucei: growth differences in different mammalian sera are not due to the species-specificity of transferrin. Experimental Parasitology, 109 (3): 188 - 194.
Pays: Laboratory of Molecular Parasitology, IBMM, Free University of Brussels, 12, rue des Professeurs Jeener et Brachet, B-6041 Gosselies, Belgium.
13271 Schimanski, B., Ma, L.Y. & Günzl, A., 2004. Failure to detect binding of Trypanosoma brucei SNAPc to U2 and U6 snRNA gene sequences by in vitro transcription competition and pull-down assays. Molecular and Biochemical Parasitology, 137 (2): 293 - 296.
Günzl: Center for Microbial Pathogenesis, University of Connecticut Health Center, 263 Farmington Avenue, Farmington, CT 06030-3710, USA.
13272 Schlecker, T., Schmidt, A., Dirdjaja, N., Voncken, F., Clayton, C. & Krauth-Siegel, R.L., 2005. Substrate specificity, localization, and essential role of the glutathione peroxidase-type tryparedoxin peroxidases in Trypanosoma brucei. Journal of Biological Chemistry, 280 (15): 14385 - 14394.
Krauth-Siegel: Biochemie-Zentrum der Universität Heidelberg, Im Neuenheimer Feld 504, 69120 Heidelberg, Germany. [[email protected]]
13273 Semballa, S., Geffard, M., Daulouede, S., Malvy, D., Veyret, B., Lemesre, J.L., Holzmuller, P., Mnaimneh, S. & Vincendeau, P., 2004. Antibodies directed against nitrosylated neoepitopes in sera of patients with human African trypanosomiasis. Tropical Medicine and International Health, 9 (10): 1104 - 1110.
Semballa: Laboratoire de Parasitologie, Université de Bordeaux II, Bâtiment 1b, 33076 Bordeaux Cedex, France.
13274 Shi, H.F., Chamond, N., Tschudi, C. & Ullu, E., 2004. Selection and characterization of RNA interference-deficient trypanosomes impaired in target mRNA degradation. [T. brucei] Eukaryotic Cell, 3 (6): 1445 - 1453.
Ullu: Department of Internal Medicine, Yale Medical School, BCMM 136D, 295 Congress Ave., New Haven, CT 06536-8012, USA. [[email protected]]
13275 Shi, H.F., Ullu, E. & Tschudi, C., 2004. Function of the trypanosome Argonaute 1 protein in RNA interference requires the N-terminal RGG domain and arginine 735 in the Piwi domain. Journal of Biological Chemistry, 279 (48): 49889 - 49893.
Tschudi: Department of Epidemiology and Public Health, Yale University Medical School, 295 Congress Ave., New Haven, CT 06536-0812, USA. [[email protected]]
13276 Smith, T.K., Crossman, A., Brimacombe, J.S. & Ferguson, M.A.J., 2004. Chemical validation of GPI biosynthesis as a drug target against African sleeping sickness. EMBO Journal, 23 (23): 4701 - 4708.
Ferguson: Division of Biological Chemistry and Molecular Microbiology, The Wellcome Trust Biocentre, School of Life Sciences, University of Dundee, Dundee DD1 5EH, UK. [[email protected]]
13277 Stuart, K.D., Schnaufer, A., Ernst, N.L. & Panigrahi, A.K., 2005. Complex management: RNA editing in trypanosomes. Trends in Biochemical Sciences, 30 (2): 97 - 105.
Stuart: Seattle Biomedical Research Institute, 307 Westlake Avenue North, Suite 500, Seattle, WA 98109 USA. [[email protected]]
13278 Tu, X.M. & Wang, C.C., 2005. Pairwise knockdowns of cdc2-Related Kinases (CRKs) in Trypanosoma brucei identified the CRKs for G1/S and G2/M transitions and demonstrated distinctive cytokinetic regulations between two developmental stages of the organism. Eukaryotic Cell, 4 (4): 755 - 764.
Wang: Department of Pharmaceutical Chemistry, UCSF, San Francisco, CA 94143-2280 USA. [[email protected]]
13279 Uzcategui, N.L., Szallies, A., Pavlovic-Djuranovic, S., Palmada, M., Figarella, K., Boehmer, C., Lang, F., Beitz, E. & Duszenko, M., 2004. Cloning, heterologous expression, and characterization of three aquaglyceroporins from Trypanosoma brucei. Journal of Biological Chemistry, 279 (41): 42669 - 42676.
Duszenko: Physiologisch-chemisches Institut, Universität Tübingen, Hoppe-Seyler Str. 4, 72076 Tübingen, Germany. [[email protected]]
13280 Vondrušková, E., van den Burg, J., Zíková, A., Ernst, N.L., Stuart, K., Benne, R. & Lukeš, J., 2005. RNA interference analyses suggest a transcript-specific regulatory role for mitochondrial RNA-binding proteins MRP1 and MRP2 in RNA editing and other RNA processing in Trypanosoma brucei. Journal of Biological Chemistry, 280 (4): 2429 - 2438.
Lukes: Institute of Parasitology, Czeck Academy of Sciences, University of South Bohemia, 37005 Ceské Budejovice, Czech Republic. [jula@ paru.cas.cz]
13281 Walgraffe, D., Devaux, S., Lecordier, L., Dierick, J.-F., Dieu, M., Abbeele, J. van den, Pays, E. & Vanhamme, L., 2004. Characterization of subunits of the RNA polymerase I complex in Trypanosoma brucei. Molecular and Biochemical Parasitology, 139 (2): 249 - 260.
Pays: Laboratory of Molecular Parasitology, Department of Molecular Biology, IBMM, Free University of Brussels, 12, rue des Professeurs Jeener et Brachet, B-6041 Gosselies, Belgium.
13282 Walker, R., Jr., Saha, L., Hill, G.C. & Chaudhuri, M., 2004. The effect of over-expression of the alternative oxidase in the procyclic forms of Trypanosoma brucei. Molecular and Biochemical Parasitology, 139 (2): 153 - 162.
Chaudhuri: Department of Microbiology, Meharry Medical College, Nashville, TN 37208, USA.
13283 Witola, W.H., Sarataphan, N., Inoue, N., Ohashi, K. & Onuma, M., 2005. Genetic variability in ESAG6 genes among Trypanosoma evansi isolates and in comparison to other trypanozoon members. Acta Tropica, 93 (1): 63 - 73.
Onuma: Laboratory of Infectious Diseases, Graduate School of Veterinary Medicine, Hokkaido University, Sapporo 060-0818, Japan.
