In Figure  2c, by assuming that the incoming heat energy is positive and the outgoing heat energy is negative, we have (8) Taking into account a system of linear equations for the node (i, j) composed of Equations 2, 7, and 8, the temperature at any mesh node can be obtained. Finally, by substituting the above obtained IWP-2 price current density in any mesh segment and temperature at any mesh node into Equation 4, the temperature distribution in any mesh segment can be monitored. A synopsis of the corresponding

computational algorithm [27] is provided as below. Initially, a small value is assigned to the input current I. SAR302503 The corresponding maximum temperature in the mesh T max can be identified, which rises with the increasing I. By gradually increasing I with increment ΔI

to make T max reach T m, the first mesh segment melts and breaks from an arbitrary small force occurring in actual operation (e.g., vibration). At that time, the input current and the voltage between node (0, 0) and node (9, 0) are recorded as melting current STA-9090 order I m and melting voltage V m. The corresponding resistance R m of the mesh can be calculated by dividing V m by I m. It should be noted that ΔI must be small enough so that melting segment can melt one by one as far as possible. Subsequently, an ultra-small value is assigned to the cross-sectional area of the first melted mesh segment in order to approximate zero. The pathway of the current and heat in the mesh is therefore renewed. By repeating the aforementioned process, the current triggering the melting of mesh segment one by one can be obtained until the mesh becomes open. Therefore, the relationship between I m and V m as well as the variation of R m with the number n b of the broken mesh segments can be obtained click here over the entire melting process of the mesh. Results and discussion

Melting behavior of the Ag microwire mesh As shown in Figure  3a,b, the obtained relationship of melting current I m and melting voltage V m as well as the variation of mesh resistance R m with the number n b of broken mesh segments during the entire melting process of the Ag microwire mesh is compared with those of the corresponding Ag nanowire mesh, respectively. Figure 3 Comparison of melting process for both meshes. (a) The relationship between I m and V m, and (b) the variation of R m with n b . Obviously, a repetitive zigzag pattern is observed in the relationship of I m and V m in the Ag microwire mesh, which demonstrates the repetition of three different trends: increase of both I m and V m, decrease of both I m and V m, and decrease of I m but increase of V m. Such pattern in the melting behavior of Ag microwire mesh is similar with that of the corresponding Ag nanowire mesh [27].

PubMedCrossRef 5. Shah RR. Drug-induced QT interval prolongation: does ethnicity of the thorough QT study population matter? Br J Clin Pharmacol. 2013;75(2):347–58.PubMedCentralPubMedCrossRef 6. Malik M, Farbom P, Batchvarov V, Hnatkova K, Camm AJ. Relation between QT and RR intervals is highly individual among healthy subjects: implications for heart rate correction of the QT interval. Heart. 2002;87(3):220–8.PubMedCentralPubMedCrossRef 7. Desai M, Li L, Desta Z, Malik M, Flockhart D. Variability of heart rate

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of moxifloxacin-induced QTc effect. J Biopharm Stat. 2010;20(3):497–507.PubMedCrossRef”
“Key Points This study was an observational registry enrolling 315 patients treated by 46 specialists in hypertension clinics across Portugal. Patients received INCB28060 in vivo lercanidipine/enalapril (10/20 mg) fixed-dose combination (FDC) for ~2 months, and efficacy and safety of the treatment were assessed. Treatment with lercanidipine/enalapril FDC was associated with significant reductions from baseline in systolic and diastolic blood pressure (BP), and increases in the rate of BP control (<140/90 mmHg). pheromone The lercanidipine/enalapril FDC had an excellent safety profile in this population, with treatment-emergent adverse events reported in only one patient. These results suggest that lercanidipine/enalapril (10/20mg) FDC is an effective and safe treatment for the general hypertensive population in Portugal. 1 Introduction It is well recognized that arterial hypertension is a leading cause of death and disability worldwide [1]. Hypertension is a significant risk factor for cardiovascular disease, stroke, peripheral vascular disease, and end-stage renal disease [2].

Bone 47:413–423PubMedCrossRef 25. Taku K, Melby MK, Takebayashi J, Mizuno S, Ishimi Y, Omori T, Watanabe S (2010) Effect of soy isoflavone extract supplements on bone mineral density in menopausal women: meta-analysis of randomized NSC 683864 concentration controlled trials. Asia Pac J Clin Nutr 19:33–42PubMed 26. Gallagher JC, Satpathy R, Rafferty K, Haynatzka V (2004) The effect of soy protein isolate on bone metabolism. Menopause 11:290–298PubMedCrossRef 27. Kreijkamp-Kaspers S, Kok L, Grobbee DE, de Haan EH, Aleman A, Lampe JW, van der Schouw YT (2004) Effect of soy protein containing Akt inhibitor isoflavones on cognitive function, bone mineral density, and plasma lipids in postmenopausal

women: a randomized controlled trial. JAMA 292:65–74PubMedCrossRef 28. Arjmandi BH, Lucas EA, Khalil DA, Devareddy L, Smith BJ, McDonald J, Arquitt AB, Payton ME, Mason C (2005) One year soy protein supplementation has positive effects on bone formation markers but not bone density in postmenopausal women. Nutr J 4:8PubMedCrossRef 29. Wu J, Oka J, Tabata I, Higuchi

M, Toda T, Fuku N, Ezaki J, Sugiyama F, Uchiyama S, Yamada K, Ishimi Y (2006) Effects of isoflavone and exercise on BMD and fat mass in postmenopausal Japanese women: a 1-year LY294002 randomized placebo-controlled trial. J Bone Miner Res 21:780–789PubMedCrossRef 30. Evans EM, Racette SB, Van Pelt RE, Peterson LR, Villareal DT (2007) Effects of soy protein isolate and moderate exercise on bone turnover and bone mineral density in postmenopausal women. Menopause 14:481–488PubMedCrossRef 31. Brink E, Coxam V, Robins S, Wahala K, Cassidy A, Branca F (2008) Long-term consumption of isoflavone-enriched foods does not affect bone mineral density, Thiamine-diphosphate kinase bone metabolism, or hormonal status in early postmenopausal women: a randomized, double-blind, placebo controlled study. Am J Clin Nutr 87:761–770PubMed 32. Kenny AM, Mangano KM, Abourizk RH, Bruno RS, Anamani DE, Kleppinger A, Walsh SJ, Prestwood KM, Kerstetter JE (2009) Soy proteins and isoflavones affect bone mineral density

in older women: a randomized controlled trial. Am J Clin Nutr 90:234–242PubMedCrossRef 33. Vupadhyayula PM, Gallagher JC, Templin T, Logsdon SM, Smith LM (2009) Effects of soy protein isolate on bone mineral density and physical performance indices in postmenopausal women—a 2-year randomized, double-blind, placebo-controlled trial. Menopause 16:320–328PubMedCrossRef 34. Alekel DL, Van Loan MD, Koehler KJ, Hanson LN, Stewart JW, Hanson KB, Kurzer MS, Peterson CT (2010) The soy isoflavones for reducing bone loss (SIRBL) study: a 3-y randomized controlled trial in postmenopausal women. Am J Clin Nutr 91:218–230PubMedCrossRef 35. Weaver CM, Cheong JM (2005) Soy isoflavones and bone health: the relationship is still unclear. J Nutr 135:1243–1247PubMed 36. Lydeking-Olsen E, Beck-Jensen JE, Setchell KD, Holm-Jensen T (2004) Soymilk or progesterone for prevention of bone loss—a 2 year randomized, placebo-controlled trial. Eur J Nutr 43:246–257PubMedCrossRef 37.

Due to the historical nomenclature, to the absence of other comprehensive studies including all strain types and typing methods, to the inability of several techniques to distinguish between Type I and III and to the genetic and phenotypic similarities found between them in previous studies, we propose that S- and C-type nomenclature could be used to denote the two

major groups or PF-6463922 supplier lineages and the Type I and III used to distinguish subtypes within S-type strains as we have BIBW2992 chemical structure done in this paper. In agreement with previous studies both PFGE and IS900-RFLP revealed little heterogeneity between isolates of the S subtype I. By comparison, this study shows that strains of S subtype III are more polymorphic. Diverse genotypes clustered within S subtype III have been identified circulating in small regional areas in Spain or even in the same farm [34], making more evident the higher heterogeneity of these strains. Interestingly, as far as we know no evidence of S subtype I strains has been found in Spain, a country with a significant sample of S-type strains in our panel and in previous works

[8, 16]. For molecular epidemiology (i.e. strain tracking), of the typing techniques used MIRU-VNTR would be the preferred technique for studying S-type strains. This technique gave a high discriminatory index with the eight loci employed in this study and could segregate the different members of MAC and the Map S- and C-type strains, although it has limitations in that it cannot differentiate between the subtypes I and III. For detecting genetic variability between S-type strains the number CFTRinh-172 chemical structure of loci used could be reduced to 3 (292, X3 and 25). The greatest genetic variation occurred at locus 292 with S-type strains typically having a much higher number of repeats than C-type strains through (up to 11 were detected in this study). No more than 4 repeats at locus 292 were detected in C-type strains. The locus 292 locus is flanked by loci MAP2920c and MAP2921c referenced

as acetyltransferase and quinone oxidoreductase, respectively. There has been only one other report of MIRU-VNTR typing of S-type strains [22]. In the latter study MIRU-VNTR loci 3 and 7 were thought to be of special importance for identifying subtype III strains but only two subtype III strains were typed. In our study all 14 subtype III and 10 subtype I strains had the same, one-repeat unit alleles at each of these two loci, as found in the two strains typed previously [22]. Although uncommon, a few C-type strains in this study were also found with a single copy at these loci so this is even not unique to S-type strains. All Mah, Maa and Mas strains tested in this study also had one repeat unit at locus 3 and all Maa and 61% of Mah strains had a single copy at locus 7. The discriminatory power of MIRU-VNTR to differentiate between the subtypes I and III could be improved by identifying additional loci.

We use the term fungal community or mycota aware that we isolated only part of the culturable fungi and missed uncultivable fungal species. Amplification and sequencing of the fungal isolates ITS1-5.8S-ITS2 rDNA (ITS) region Amplification and sequencing of the ITS of the fungal isolates was performed with the primers ITS1F (or ITS1) and ITS4 (the sequences of these primers are available at: http://​www.​biology.​duke.​edu/​fungi/​mycolab/​primers.​htm). Direct PCR was performed using a sterile pipetor tip (10 μl) to transfer aseptically a very small amount of mycelium in a PCR tube and to squash it manually with the tip in the

PCR mix (25 μl mix, reagents and conditions XAV-939 of the Taq PCR core kit (QIAGEN, Sepantronium clinical trial Inc., Valencia, California, USA). Sequencing used the amplification primers, reagents and conditions of the BigDye ® Terminator v3.1 Cycle sequencing Kit and an automated capillary sequencer ABI 3700 DNA analyzer (Perkin Elmer, Applied Biosystems, Foster City, CA, USA). Fungal diversity and species accumulation curves Nomenclatural issues follow Mycobank. We estimated the species

diversity in asymptomatic, esca-symptomatic, and nursery plants by calculating the Simpson index of the fungal community identified in each plant sample. The community composition was assessed based on the relative abundance of species in the culturable part of the fungal community. The expected total species diversity in the different plant categories was estimated by resampling the available plant samples. Based on 1000 replicates without replacement, we calculated the total recovered diversity within each plant category. Species accumulation much curves were estimated using the vegan package implemented in the R statistical software (R Development Core Team 2006). Principal component analyses (PCA) A principal component analysis was performed in order to eventually identify differentiated fungal communities XMU-MP-1 cell line between symptomatic, asymptomatic and nursery plants. Each plant was considered as an independent replicate and the isolated fungal community on each plant

sample was recoded as presence-absence data. We assessed the fungal community based on incidence data rather than on relative frequencies to reduce the bias introduced by species that may be more easily brought into culture than others. The R package vegan was used to calculate the main ordination axes 1 and 2 based on Euclidean distances (R Development Core Team 2006). Biplots were produced based on the PCA to show both the relationship of the fungal species and the plant samples in respect to the main axes. Results Delimitation and classification of the operational taxonomic units (OTUs) based on ITS sequences of the fungal isolates The isolates were grouped based on their vegetative macro-morphology.

Alveolar macrophages are reported to transport spores out of the lungs to regional lymph nodes [4–7]. Dendritic cells have also been implicated in the rapid carriage of spores to the draining lymph nodes [8, 9]. Finally, alveolar epithelial cells have recently been

demonstrated to internalize spores both in vitro and in vivo [10–12], and have been proposed to facilitate the transcytosis of B. anthracis across the epithelial barrier. Taken together, these findings suggest that B. anthracis may escape CHIR98014 order the lungs by several distinct mechanisms. To characterize the interaction of B. anthracis spores with host cells during the early stages of inhalational anthrax, in vitro models of infection have been widely implemented [8, 13–22]. The tractability of in vitro models

has facilitated new insights into the molecular and cellular basis of spore binding and uptake, as well as host cell responses. Nonetheless, the use of in vitro models has resulted in a striking lack of consensus as to the responses and fates of both intracellular B. anthracis and infected cells. Luminespib in vitro Although there are multiple reports of germinated spores within host cells [13, 15, 16, 20, 23], several studies have indicated that germinated spores ultimately kill macrophages [13, 19, 20], while others have reported that macrophages readily kill intracellular B. anthracis [21, 22]. The lack of consensus may be due, in part, to fundamental differences between the

infection models used by research groups, which includes variability in bacterial strains, mammalian cells, and experimental conditions employed. An important issue that is likely to directly influence the outcome of in vitro models of infection is the germination state of spores as they are internalized into host cells. Several in vivo lines of evidence support the idea that spores remain dormant in the alveolar spaces of the lungs prior to uptake. First, dormant spores have been recovered from the lungs of animals several months after initial infection [7, 24]. Second, all RAS p21 protein activator 1 spores collected from the bronchial alveolar fluids of spore-infected Balb/c mice were found to be dormant [5, 23]. In contrast, a substantial percentage of intracellular spores recovered from alveolar macrophages were germinated [23]. Third, real time in vivo imaging failed to detect germinated spores within lungs, despite the effective delivery of dormant spores to these Selleck GSK2126458 organs [25–27]. One of these studies [25] reported that vegetative bacteria detected in the lungs during disseminated B. anthracis infection arrived at the lungs via the bloodstream, rather than originating from in situ spore growth. Finally, using spores that had been engineered to emit a bioluminescent signal immediately after germination initiation, a recent study reported that germination was commenced in a mouse model of infection only after spore uptake into alveolar macrophages [6].

The reason is that with the decrease of the nanoparticle size, the resonance peak will shift towards the shorter wavelength and uniform size will cause narrow extinction bands [31], which correspond to our experimental results. Supporting evidence for the function of MW of PVP In this section, we show the reason why PVP can affect the selleckchem silver nanostructure, and it is because PVP prefers to adsorb on the (100) facets of silver nanocrystals in EG [32].

The see more interaction process can be given by Equation 1. To determine the strength of adsorption between Ag+ ions and different PVPs, we resort to FT-IR analysis. Figure 5 presents the FT-IR spectra of pure PVP and Ag/PVP. In the spectra of pure PVP, the absorption peak locates at around 1,660 cm-1 Angiogenesis inhibitor ascribed to the stretching vibration of C = O which is slightly dependent on the MW of PVP. Compared with the free C = O stretching band of pure PVP, the adsorption peaks of Ag/PVP all shift towards the lower wave number due to the coordination between Ag+ ions and carbonyl oxygen. The positions of free and coordinated C = O bands in Ag/PVP with four kinds of MW are shown in Table 2. Because the strength of the coordination interaction between Ag+ ions and PVP can be estimated in terms of the magnitude

of band shifts [33], the sequence of the strength of the coordination interaction between Ag+ ions and PVP occurs as follows: second PVPMW=1,300,000 > PVPMW=40,000 > PVPMW=8,000 > PVPMW=29,000.

The larger extent of blue shift band indicates a stronger selective adsorption on the (100) facets of silver nanocrystals, which is one of the important factors giving rise to the different morphologies of silver nanocrystals produced with different PVPs. As can be seen in Figure 5a,c,d, there is a peak at about 880 cm-1 assigned to the breathing vibration of the pyrrolidone ring, indicating that the pyrrolidone ring may be tilted on the surface of silver nanowires [34]. In addition, in these three figures, the peak at 2,970 cm-1 ascribed to asymmetric stretching vibration of CH2 in the skeletal chain of PVP, which implies that the CH2 chain is close to the surface of silver nanowires. Therefore, the conformation of PVP makes the fine and close adsorption on the (100) facets of silver nanocrystals. Conversely, both peaks in Figure 5b are weak, leading to the formation of high-yield silver nanospheres which is consistent with the result shown in Figure 1b. (1) Figure 5 FT-IR spectra of pure PVP and Ag/PVP with different MWs. (a) MW = 8,000. (b) MW = 29,000. (c) MW = 40,000. (d) MW = 1,300,000. Table 2 Positions of free and coordinated C = O bands in Ag/PVP with four kinds of MWs System MW   8,000 29,000 40,000 1,300,000 FT-IR (cm-1) 1,640 1,644 1,636 1,633 Redshift (cm-1) 20 16 24 27 Another factor influencing the morphology of silver nanocrystals with different PVPs is the steric effect.

At 4°C, FITC-EGF was bound to the cell surface. In both DMSO- and analogue 20-treated cells, EGF was internalized and showed a similar intracellular distribution

for up to 1 h, indicating that the compound does not inhibit endocytosis or protein LY2603618 manufacturer transport in the early endocytic pathway. After > 3 h, most of internalized FITC-EGF had disappeared from cells treated with DMSO, indicating it was degraded in lysosomes (Figure 10A). In contrast, cells treated with analogue 20 showed significantly more cytoplasmic punctate FITC-EGF, indicating that the compound interferes with the lysosomal delivery and/or degradation of internalized EGF. Figure 10 Motuporamines inhibit the degradation of internalized FITC-EGF and causes intracellular accumulation of EGFR. (A) Cells labelled with FITC-EGF at 4°C were exposed to DMSO (control) or 5 μM analogue 20

(motuporamine) for 0, 30 min or 6 h at 37°C, and FITC-EGF was visualized by fluorescence AZD0156 clinical trial microscopy. (B) Cells were exposed to DMSO (control) or 5 μM analogue 20 for 24 h at 37°C, and EGFR was visualized by immunofluorescence microscopy. To examine the effect of the compound on EGFR localization, cells were exposed to DMSO or dhMotC and the Apoptosis Compound Library cell assay localization of EGFR was determined by immunofluorescence microscopy. In control cells, EGFR was present at the plasma membrane, with a noticeable concentration at the leading edge of migrating cells, as well as in intracellular structures (Figure 10B). In cells treated with dhMotC, EGFR was present in intracellular punctate structures and there was a clear

reduction in plasma membrane-associated EGFR (Figure 10B), indicating that the compound interfered with the lysosomal delivery and/or degradation Sucrase of internalized EGFR. Conclusion A first screen of differential sensitivity of ρ + and ρ 0 cells showed that most drugs, including the therapeutic azole antifungals, do not require mitochondrial function to exert their growth inhibitory effects. Since ρ 0 cells appear incapable of generating ROS [35–38], ROS production by mitochondria is probably not a primary determinant of the mechanism of action of most antifungal agents. Only 4 chemicals required functional mitochondria to inhibit yeast growth. Antimycin A inhibits the transfer of electrons from ubiquinol to the cytochrome bc(1) complex. This inhibition is well known to cause the leakage of electrons to oxygen, resulting in the release of ROS [39]. Therefore, the inability of antimycin A to inhibit growth in ρ 0 cells can be attributed to the lack of ROS production due to the absence of a respiratory chain. Unexpectedly, ρ 0 cells were also resistant to 3 chemicals that target sphingosine and ceramide synthesis. Using dhMotC as an example, we showed that yeast cell killing requires holocytochrome c synthase activity.

The child’s sex was obtained at the time of birth, and the child’s birth weight, gestational age and the mother’s age at delivery were abstracted from obstetric records. In the questionnaire administered at 18 weeks’ gestation, the mother was asked how many hours per week she spent engaging in strenuous GM6001 manufacturer physical activity. The questionnaire also asked the number of hours per week the mother spent in a number of specific types of leisure activity, each of which was assigned a MET score [12], and a weighted activity index was developed by

multiplying the MET score by the number of hours of activity per week. Dietary information for the mothers was obtained from a food frequency questionnaire administered at 32 weeks’ gestation which asked how often they consumed each of the 43 food groups. Using nutrient information on standard-sized EPZ015938 order portions, the mother’s total weekly energy, carbohydrate, fat and protein intakes were derived [13]. Although the main analysis did not adjust for these variables, since the equivalent paternal information was not available, an additional analysis was performed in which the relationships of maternal smoking in pregnancy with offspring bone outcomes were adjusted for maternal physical activity (strenuous activity

of 3 h or more per week and weighted activity index) and diet (weekly energy, carbohydrate, fat and protein intake) during pregnancy. Pubertal stage data for selleck inhibitor the children were obtained from Tanner stage questionnaires administered to the parents at 116 months and were based on pubic hair development for boys and breast development for girls, or pubic hair development if this was unavailable. For girls, age at Immune system menarche was derived from a series of questionnaires administered between the ages of 8 and 17 years which asked if the daughter had started her menstrual periods and, if so, the age she was at her first menstrual period. Where there was disagreement between questionnaires, the age given on the earliest questionnaire was used. Most children (99% of boys and 96% of girls) with pubertal stage information were either pre- or

early pubertal (Tanner stage 1 or 2). For this reason, and due to the high proportion of missing pubertal stage data, this has not been adjusted for in the main regression analysis, but an additional analysis was performed which adjusted for pubertal stage and, for girls, whether menarche occurred at age ≤10 years. Paternity If, when asked in a questionnaire administered in pregnancy, the mother had not confirmed her partner to be the child’s biological father, all paternal information (smoking status, BMI, age, height and education) was treated as missing. Statistical analysis We assessed maternal and paternal smoking associations with offspring bone outcomes separately and also in combined mutually adjusted regression models.

In intermediate forms (figures 5F and 6F, arrowheads) and trypomastigotes (figures 5 and 6I–L), TcKap4 and TcKap6 were find more distributed mainly at the periphery of the kDNA network. In order to better understand the kDNA arrangement present in the intermediate forms and the distribution of KAPs in the different developmental stages of T. cruzi, ultrastructural analyses and immunocytochemistry assays were performed (figure 7). In epimastigotes and amastigotes (figure 7A and 7D, respectively), which present a disk-shaped

kinetoplast, we could observe gold particles distributed throughout the kinetoplast disk when both antisera were used (figure 7B and 7E for TcKAP4 and 7C and 7F for TcKAP6). In intermediate forms, which present an enlarged kinetoplast when compared to the disk-shaped kinetoplast of amastigotes (figure 7G), labeling of TcKAPs is more intense at the peripheral region than in the central area (figure 7H and 7I). In trypomastigotes, which present a round-shaped kinetoplast (figure 7J), gold particles were mainly observed at the periphery of the kinetoplast network (figure 7K and 7L), confirming the results obtained by immunofluorescence analysis. Preliminary cytochemical studies had already shown different distributions of basic selleckchem proteins in the kinetoplasts of the different developmental stages of T. cruzi [41]. However, the reason for this differential protein distribution remain unclear.

It is possible that these basic proteins are involved in topological rearrangements of the kDNA network during the T. cruzi life cycle, in which the compact bar-shaped kinetoplast is converted into a globular structure. However, no data are currently available to confirm or refute this hypothesis. Figure 5 Distribution of TcKAP4 in T. cruzi. Immunolocalization of TcKAP4 in epimastigotes (A-D), amastigotes/intermediate forms (E-H) and trypomastigotes (I-L) of T. cruzi. In epimastigotes (B) and amastigotes (F-arrow), the protein is distributed throughout the kDNA disk (insets). In intermediate forms (F-arrowhead) and trypomastigotes

(J-inset), a peripheral labeling of the kinetoplast was observed. (A-E-I) Phase-contrast image, (B-F-J) fluorescence not image using anti-TcKAP4 serum, (C-G-K) propidium iodide showing the Selleck DMXAA nucleus (n) and the kinetoplast (k), and (D-H-L) the overlay image. Bars = 5 μm. Figure 6 Distribution of TcKAP6 in T. cruzi. Immunolocalization of TcKAP6 in epimastigotes (A-D), amastigotes/intermediates forms (E-H) and trypomastigotes (I-L) of T. cruzi. As observed for TcKAP4, this protein was also distributed throughout kDNA disk in epimastigotes (B-inset) and amastigotes (F-arrow and inset), and at the periphery of the kinetoplast in intermediate forms (F-arrowhead) and trypomastigotes (J-inset). (A-E-I) Phase-contrast image, (B-F-J) location of TcKAP6 in the kinetoplasts of T. cruzi, (C-G-K) iodide propidium labeling and (D-H-L) the overlay image. k = kinetoplast, n = nucleus. Bars = 5 μm.