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81 results for “Trypanosoma cruzi”
Fig. 3 in Trypanosoma madeirae sp. n.: A species of the clade T. cruzi associated with the neotropical common vampire bat Desmodus rotundus
Fig. 3. Phylogenetic positioning of T. rotundus in the clade T. cruzi. ML phylogenetic analysis based on the concatenated sequences of V7V8 SSU rRNA and gGAPDH genes (1.690 characters, –Ln = 8768.346166) from ten isolates of T. rotundus, other 29 bat trypanosomes, and 21 trypanosomes from other mammals. T. lewisi was used as outgroup. The numbers at the nodes correspond respectively to P, ML (500 replicates) and BI support values.
Fig. 2 in Trypanosoma madeirae sp. n.: A species of the clade T. cruzi associated with the neotropical common vampire bat Desmodus rotundus
Fig. 2. Barcoding (V7-V8 SSU rRNA sequences) of T. rotundus from cultures and bat blood samples, and its related species of the clade T. cruzi. Phylogenetic tree inferred by Parsimony using 93 (∼800 bp) of V7-V8 SSU rRNA sequences. The node numbers are bootstrap values derived from 500 replicates.
Fig. 1 in Trypanosoma madeirae sp. n.: A species of the clade T. cruzi associated with the neotropical common vampire bat Desmodus rotundus
Fig. 1. Geographical origin of Trypanosoma rotundus n. sp. isolates obtained by hemoculturing and archived blood samples from Desmodus rotundus captured in the following Brazilian states: PA, Pará; MG, Minas Gerais; ES, Espírito Santo; RJ, Rio de Janeiro; SP, São Paulo and SC, Santa Catarina.
Fig. 4 in Trypanosoma madeirae sp. n.: A species of the clade T. cruzi associated with the neotropical common vampire bat Desmodus rotundus
Fig. 4. Photomicrographs illustrative of the morphological diversity of culture forms of T. madeirae (isolate M3-209). (a) rosetes of epimastigotes, (b-d) flagellates resembling promastigotes forms, (d-h) epimastigotes (7 days), (i-k) large epimastigote forms under division, (l-m), large trypomastigotes, and (n) slender trypomastigotes (10 days). Giemsa stained. 1000x. K, kinetoplast, N, nucleus, F, flagellum. The scale bar indicates 10 μm.
Trypanosoma cruzi DM28c_2018 annotation with UTR
<p>UTR regions were annotated to the T. cruzi genome 2018 (https://tritrypdb.org/common/downloads/release-68/TcruziDm28c2018/gff/data/). We used custom script for the 5' UTR and peaks2UTR - https://academic.oup.com/bioinformatics/article/39/3/btad112/7067741 for the process. </p>
Figure 7. T in Bioinformatics and expression analysis of the Xeroderma Pigmentosum complementation group C (XPC) of Trypanosoma evansi in Trypanosoma cruzi cells
Figure 7. T. cruzi growth assessment after cisplatin treatment (300 ΜM). (a) Wild type (WT). (b) TcXPC superexpressor (Tc-TcXPC). (c) TevXPC expressor (Tc-TevXPC). The solid lines represent the untreated cells, while the dotted lines represent the cells treated with cisplatin. Statistical student's t test: (*) On that point, cells treated with cisplatin presented a statistically significant lower growth in relation to untreated cells (p <0.05). Representative results of three independent experiments.
Figure 6 in Bioinformatics and expression analysis of the Xeroderma Pigmentosum complementation group C (XPC) of Trypanosoma evansi in Trypanosoma cruzi cells
Figure 6. Growth assessment of T. cruzi: wild type (WT), TcXPC superexpressor (Tc-TcXPC) and TevXPC expressor (Tc-TevXPC). Statistical student's t test: (*) On that point, only Tc-TevXPC presented a statistically significant lower growth in relation to WT (p <0.05); (**) On that point, both Tc-TcXPC and Tc-TevXPC presented a significant lower growth in relation to WT (p <0.05). All parasites were at same initial concentration, grown on LIT medium and were counted daily. Representative results of three independent experiments.
Figure 5 in Bioinformatics and expression analysis of the Xeroderma Pigmentosum complementation group C (XPC) of Trypanosoma evansi in Trypanosoma cruzi cells
Figure 5. TevXPC amplification by RT-PCR with the cDNA from cell cultures. Lanes: (1) 1Kb DNA Ladder; (2) WT; (3) Tc-TcXPC; (4 and 5) Tc-TevXPC; (6) positive control (DNA from T. evansi); (7) negative control.
Figure 4 in Bioinformatics and expression analysis of the Xeroderma Pigmentosum complementation group C (XPC) of Trypanosoma evansi in Trypanosoma cruzi cells
Figure 4. (a) TcXPB-R protein model. (b) TevXPB-R protein model. (c) TcXPB-R (blue) and TevXPB-R (orange) models overlay.
Figure 2 in Bioinformatics and expression analysis of the Xeroderma Pigmentosum complementation group C (XPC) of Trypanosoma evansi in Trypanosoma cruzi cells
Figure 2. (a) Alignment between TcXPC and TevXPC proteins (mismatches highlighted) and its domains. Green: RAD4/PNGase transglutaminase-like fold. Blue: RAD4 beta-hairpin domain 1. Red: RAD4 beta-hairpin domain 2. Yellow: RAD4 beta-hairpin domain 3. (b) Candidate sequence motif involved in p62 interaction (highlighted by brown rectangle) found in TcXPC and TevXPC. This sequence is suggested based on the sequence motif described for Human XPC and yeast RAD4: D/E-F/W-E-D/E-V.
Figure 1 in Bioinformatics and expression analysis of the Xeroderma Pigmentosum complementation group C (XPC) of Trypanosoma evansi in Trypanosoma cruzi cells
Figure 1. (a) TcXPC protein model. (b) TevXPC protein model. (c) TbXPC protein model (d) Model of TevXPC protein bound to a mismatch DNA. (e) TcXPC (red), TevXPC (blue) and TbXPC (green) models overlay. (f) Crystal structure of Rad4-Rad23 bound to a mismatched DNA performed by Min and Pavletich (2007).
Figure 3 in Bioinformatics and expression analysis of the Xeroderma Pigmentosum complementation group C (XPC) of Trypanosoma evansi in Trypanosoma cruzi cells
Figure 3. (a) TcXPB protein model. (b) TevXPB protein model. (c) TcXPB (green) and TevXPB (red) models overlay.
Fig. 3 A in Comparative analysis of metacyclogenesis and infection curves in different discrete typing units of Trypanosoma cruzi
Fig. 3 A The production of amastigotes per cell in T. cruzi infections provides insight into the intracellular dynamics of T. cruzi within host cells. B Percentage of uninfected cells observed along the infection curves, susceptibility dynamics, and infection progression, highlighting variations in the percentage of uninfected cells throughout the experimental period. C Release of cell-derived trypomastigotes during infection of Vero cells, Neubauer chamber count
Fig. 1 A in Comparative analysis of metacyclogenesis and infection curves in different discrete typing units of Trypanosoma cruzi
Fig. 1 A Microphotographs of 10-day incubation cultures of Trypanosoma cruzi epimastigotes in LIT medium with Field's staining and magnification (100 ×), metacyclic forms are indicated by red arrows. B Epimastigote production, evaluated for 12 days in a LIT medium. C Metacyclogenetic curve representing the dynamic process of metacyclic trypomastigote formation in T. cruzi. In x is the time (days) while the y-axis indicates the number of metacyclic trypomastigotes (MT) per milliliter. The data points provide information on the efficacy and kinetics of metacyclic trypomastigote production. D Dynamics of metacyclogenesis in T. cruzi, capturing both the starting point and the peak of the process. The data presented provide a better understanding of the timing and efficiency of metacyclic trypomastigote production. E This comparative approach uses brackets to indicate statistically significant differences (p <0.05) between DTUs in both the onset and peak phases of metacyclogenesis. In this graph, it can be seen whether there are DTUs with noticeable variations during the kinetics of metacyclogenesis
Fig. 2 in Comparative analysis of metacyclogenesis and infection curves in different discrete typing units of Trypanosoma cruzi
Fig. 2 Mosaic of microphotographs showing T. cruzi CDT infections in Vero cells for 120 h, using different DTUs. Samples were fixed with formaldehyde and stained with Field's stain. This representation captures the different stages and dynamics of infection in the different DTUs, and the cell morphological changes induced. White arrows indicate the presence of amastigotes at 24 h. By 72 h, amastigote nests become visible, and at 96–120 h, nests along with cell-derived trypomastigotes are observed
Fig. 3 in Cluster Analysis of Non-conserved Proteins of Trypanosoma cruzi Reference Strains Displays Parity between these Groupings (Peptidemes) and the Consensually Accepted Parasite Lineages
Fig. 3. Phenogram of the peptidemes (P) of eight Trypanosoma cruzi reference strains obtained using the SM coefficient and the UPGMA clustering algorithm, based on data from non-conserved proteins, as seen in SDS-PAGE analysis. The major peptidemes are indicated as mP 1 and mP 2. Their subgroups are identified on the right (P II, P VI, P I), and were numbered following their respective genetic types (TcII, TcVI, TcI), as currently used.
Fig. 1 in Cluster Analysis of Non-conserved Proteins of Trypanosoma cruzi Reference Strains Displays Parity between these Groupings (Peptidemes) and the Consensually Accepted Parasite Lineages
Fig. 1. Total protein profiles of eight Trypanosoma cruzi reference strains separated in 10% SDS-PAGE at 250 V, 25 mA, 90 min, and stained by Coomassie brilliant blue. The position of some conserved proteins is indicated on the right. M: molecular mass markers. (kDa) are indicated on the left.
Fig. 2 in Cluster Analysis of Non-conserved Proteins of Trypanosoma cruzi Reference Strains Displays Parity between these Groupings (Peptidemes) and the Consensually Accepted Parasite Lineages
Fig. 2. Diagrammatic representation of the twenty-two protein bands not shared by all Trypanosoma cruzi reference strains (nonconserved proteins), as visualized in SDS-PAGE. These bands were coded and analyzed by numerical taxonomy procedures. At the top is indicated the number of the major groups they belong, as identified by different approaches. The bands that were exclusive of one or more strains were highlighted with rectangles. M: molecular mass markers. (kDa) are indicated on the left.
Fig. 1 in In vitro Trypanosoma cruzi Growth Inhibition by Extremely Low-frequency Electromagnetic Fields
Fig. 1. Effect of 60 Hz sinusoidal magnetic fields at 2.0 mT and 24 h exposure on cell growth of T. cruzi epimastigote cultures. Bars represent arithmetical grouped means ± standard deviations.
Fig. 1 in High Trypanosoma cruzi infection prevalence associated with minimal cardiac pathology among wild carnivores in central Texas
Fig. 1. Spatial occurrence and distribution of T. cruzi infected, hunter-harvested wildlife, 2014. Number of infected over total number of that species tested are shown by county.
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OpenNeuro
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