Academic literature on the topic 'Erythrocytes invasion'
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Journal articles on the topic "Erythrocytes invasion"
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Klotz, F. W., J. D. Chulay, W. Daniel, and L. H. Miller. "Invasion of mouse erythrocytes by the human malaria parasite, Plasmodium falciparum." Journal of Experimental Medicine 165, no. 6 (June 1, 1987): 1713–18. http://dx.doi.org/10.1084/jem.165.6.1713.
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Plasmodium falciparum malaria merozoites require erythrocyte sialic acid for optimal invasion of human erythrocytes. Since mouse erythrocytes have the form of sialic acid found on human erythrocytes (N-acetyl neuraminic acid), mouse erythrocytes were tested for invasion in vitro. The Camp and 7G8 strains of P. falciparum invaded mouse erythrocytes at 17-45% of the invasion rate of human erythrocytes. Newly invaded mouse erythrocytes morphologically resembled parasitized human erythrocytes as shown on Giemsa-stained blood films and by electron microscopy. The rim of parasitized mouse erythrocytes contained the P. falciparum 155-kD protein, which is on the rim of ring-infected human erythrocytes. Camp but not 7G8 invaded rat erythrocytes, indicating receptor heterogeneity. These data suggest that it may be possible to adapt the asexual erythrocytic stage of P. falciparum to rodents. The development of a rodent model of P. falciparum malaria could facilitate vaccine development.
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Orwa, Titus Okello, Rachel Waema Mbogo, and Livingstone Serwadda Luboobi. "Mathematical Model for Hepatocytic-Erythrocytic Dynamics of Malaria." International Journal of Mathematics and Mathematical Sciences 2018 (July 2, 2018): 1–18. http://dx.doi.org/10.1155/2018/7019868.
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Human malaria remains a major killer disease worldwide, with nearly half (3.2 billion) of the world’s population at risk of malaria infection. The infectious protozoan disease is endemic in tropical and subtropical regions, with an estimated 212 million new cases and 429,000 malaria-related deaths in 2015. An in-host mathematical model ofPlasmodium falciparummalaria that describes the dynamics and interactions of malaria parasites with the host’s liver cells (hepatocytic stage), the red blood cells (erythrocytic stage), and macrophages is reformulated. By a theoretical analysis, an in-host basic reproduction numberR0is derived. The disease-free equilibrium is shown to be locally and globally asymptotically stable. Sensitivity analysis reveals that the erythrocyte invasion rateβr, the average number of merozoites released per bursting infected erythrocyteK, and the proportion of merozoites that cause secondary invasions at the blood phaseζare the most influential parameters in determining the malaria infection outcomes. Numerical results show that macrophages have a considerable impact in clearing infected red blood cells through phagocytosis. Moreover, the density of infected erythrocytes and hence the severity of malaria are shown to increase with increasing density of merozoites in the blood. Concurrent use of antimalarial drugs and a potential erythrocyte invasion-avoidance vaccine would minimize the density of infected erythrocytes and hence malaria disease severity.
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Baum, Jake, Margaret Pinder, and David J. Conway. "Erythrocyte Invasion Phenotypes of Plasmodiumfalciparum in The Gambia." Infection and Immunity 71, no. 4 (April 2003): 1856–63. http://dx.doi.org/10.1128/iai.71.4.1856-1863.2003.
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ABSTRACT In vitro experimentation with Plasmodium falciparum has determined that a number of different receptor-ligand interactions are involved in the invasion of erythrocytes. Most culture-adapted parasite isolates use a mechanism of invasion that depends primarily on the erythrocyte sialoglycoprotein glycophorin A (GYPA) and erythrocyte-binding antigen 175 (EBA-175) of the parasite blood-stage merozoite. However, a minority of culture-adapted parasites and a majority of Indian field isolates can apparently invade by other means. Here, erythrocyte invasion phenotypes of P. falciparum field isolates in Africa were studied. For 38 Gambian isolates, invasion of neuraminidase-treated and trypsin-treated erythrocytes was inhibited, on average, by more than 60 and 85%, respectively, indicating a high level of dependence on sialic acid and trypsin-sensitive proteins on the erythrocyte surface. These results support the hypothesis that African P. falciparum parasites use GYPA as a primary receptor for invasion. However, the considerable variation among isolates confirms the idea that alternative receptors are also used by many parasites. Three amino acid polymorphisms in the GYPA-binding region of EBA-175 (region II) were not significantly associated with invasion phenotype. There was variation among isolates in the selectivity index (i.e., a statistical tendency toward aggregation or multiple invasions of host erythrocytes), but this variation did not correlate with enzyme-determined invasion phenotype or with eba-175 alleles. Overall, these invasion phenotypes in Africa support a vaccine strategy of inhibiting EBA-175 binding to GYPA but suggest that parasites with alternative phenotypes would be selected for if this strategy were used alone.
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Tham, Wai-Hong, Danny W. Wilson, Linda Reiling, Lin Chen, James G. Beeson, and Alan F. Cowman. "Antibodies to Reticulocyte Binding Protein-Like Homologue 4 Inhibit Invasion of Plasmodium falciparum into Human Erythrocytes." Infection and Immunity 77, no. 6 (March 23, 2009): 2427–35. http://dx.doi.org/10.1128/iai.00048-09.
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ABSTRACT Plasmodium falciparum invasion into human erythrocytes relies on the interaction between multiple parasite ligands and their respective erythrocyte receptors. The sialic acid-independent invasion pathway is dependent on the expression of P. falciparum reticulocyte binding protein-like homologue 4 (PfRh4), as disruption of the gene abolishes the ability of parasites to switch to this pathway. We show that PfRh4 is present as an invasion ligand in culture supernatants as a 160-kDa proteolytic fragment. We confirm that PfRh4 binds to the surfaces of erythrocytes through recognition of an erythrocyte receptor that is neuraminidase resistant but trypsin and chymotrypsin sensitive. Serum antibodies from malaria-exposed individuals show reactivity against the binding domain of PfRh4. Purified immunoglobulin G raised in rabbits against the binding domain of PfRh4 blocked the binding of native PfRh4 to the surfaces of erythrocytes and inhibited erythrocyte invasion of parasites using sialic acid-independent invasion pathways and grown in neuraminidase-treated erythrocytes. Our results suggest PfRh4 is a potential vaccine candidate.
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Shaw, M. K., and L. G. Tilney. "The entry of Theileria parva merozoites into bovine erythrocytes occurs by a process similar to sporozoite invasion of lymphocytes." Parasitology 111, no. 4 (November 1995): 455–61. http://dx.doi.org/10.1017/s0031182000065951.
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SUMMARYThe entry of Theileria parva merozoites into bovine erythrocytes in vivo is described and compared to sporozoite invasion of lymphocytes. Merozoites make initial contact with erythrocytes with any part of their surface and invasion of the host cell does not require the re-orientation of the apical end of the merozoite towards the surface of the erythrocyte. After the initial attachment the merozoite and host cell membranes form a continual close junction with the two apposed membranes separated by a 6–8 nm gap containing moderately dense material. The progressive circumferential ‘zippering’ of these closely apposed membranes leads to the movement of the parasite into the erythrocyte. The newly internalized merozoite which is completely surrounded by the erythrocyte plasma membrane escapes from this enclosing membrane by a process involving the discharge of at least the rhoptries; whether the merozoite also contain other types of secretory organelles (e.g. micronemes, microspheres or dense bodies) remains to be determined. Morphologically, the events involved in merozoite invasion of erythrocytes are almost identical to the process of sporozoite invasion of lymphocytes but differ significantly from the entry process of the invasive stages of other Apicomplexan parasites.
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ZINTL, A., C. WESTBROOK, H. E. SKERRETT, J. S. GRAY, and G. MULCAHY. "Chymotrypsin and neuraminidase treatment inhibits host cell invasion by Babesia divergens (Phylum Apicomplexa)." Parasitology 125, no. 1 (July 2002): 45–50. http://dx.doi.org/10.1017/s0031182002001798.
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The process of host cell invasion by Babesia divergens is poorly understood and improved knowledge of the mechanism involved could lead to development of measures effective in disease prevention. To investigate parasite ligands on the erythrocyte surface, B. divergens cultures in bovine erythrocytes were transferred into enzyme-treated bovine, human, ovine and equine erythrocytes. Parasite invasion of bovine erythrocytes was not affected by trypsin treatment while treatment with alpha-chymotrypsin led to a reduction in parasite growth of 20–40%. Treatment of bovine and non-bovine erythrocytes with neuraminidase decreased their susceptibility to invasion by up to 97% implicating sialic acid as an important erythrocyte ligand for babesia, but the addition of either bovine or human N-acetylneuraminyl-lactose to B. divergens cultures in bovine erythrocytes had no inhibitory effect.
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Barnwell, J. W., M. E. Nichols, and P. Rubinstein. "In vitro evaluation of the role of the Duffy blood group in erythrocyte invasion by Plasmodium vivax." Journal of Experimental Medicine 169, no. 5 (May 1, 1989): 1795–802. http://dx.doi.org/10.1084/jem.169.5.1795.
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A short-term in vitro culture system that allows for significant re-invasion of target erythrocytes by Plasmodium vivax was used to study the role of the Duffy blood group antigen as a ligand for merozoite invasion by this human malaria species. Using human Duffy-positive and -negative erythrocytes, various primate erythrocytes, enzymatic modification of erythrocytes, and mAb that defines a new Duffy determinant (Fy6) we conclude that the erythrocyte glycoprotein carrying Duffy determinants is required as a ligand for the invasion of human erythrocytes by P. vivax merozoites. Blockade of invasion by Fab fragments of the anti-Fy6 mAb equal to that of the intact molecule and the correlation of P. vivax susceptibility with the presence of the Fy6 determinant suggests this epitope or a nearby domain may be an active site on the Duffy glycoprotein. However, as for P. knowlesi, there is evidence that an alternate pathway for P. vivax invasion of simian erythrocytes may exist.
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Schülein, Ralf, Anja Seubert, Christian Gille, Christa Lanz, Yves Hansmann, Yves Piémont, and Christoph Dehio. "Invasion and Persistent Intracellular Colonization of Erythrocytes." Journal of Experimental Medicine 193, no. 9 (May 7, 2001): 1077–86. http://dx.doi.org/10.1084/jem.193.9.1077.
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The expanding genus Bartonella includes zoonotic and human-specific pathogens that can cause a wide range of clinical manifestations. A productive infection allowing bacterial transmission by blood-sucking arthropods is marked by an intraerythrocytic bacteremia that occurs exclusively in specific human or animal reservoir hosts. Incidental human infection by animal-adapted bartonellae can cause disease without evidence for erythrocyte parasitism. A better understanding of the intraerythrocytic lifestyle of bartonellae may permit the design of strategies to control the reservoir and transmittable stages of these emerging pathogens. We have dissected the process of Bartonella erythrocyte parasitism in experimentally infected animals using a novel approach for tracking blood infections based on flow cytometric quantification of green fluorescent protein–expressing bacteria during their interaction with in vivo–biotinylated erythrocytes. Bacteremia onset occurs several days after inoculation by a synchronous wave of bacterial invasion into mature erythrocytes. Intracellular bacteria replicate until reaching a stagnant number, which is sustained for the remaining life span of the infected erythrocyte. The initial wave of erythrocyte infection is followed by reinfection waves occurring at intervals of several days. Our findings unravel a unique bacterial persistence strategy adapted to a nonhemolytic intracellular colonization of erythrocytes that preserves the pathogen for efficient transmission by blood-sucking arthropods.
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Murphy, Sean C., Souvik Bhattacharjee, Travis Harrison, and Kasturi Haldar. "Accessing the Erythrocyte Cytoplasm: A Method for Manipulating the Intracellular Environment of Erythrocytes for the Study of Malaria Invasion, Trafficking and Growth." Blood 104, no. 11 (November 16, 2004): 3688. http://dx.doi.org/10.1182/blood.v104.11.3688.3688.
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Abstract Invasion of erythrocytes by malaria parasites requires participation of both parasite ligands and host determinants. Further recent studies show that erythrocyte G protein signaling regulates malarial infection. Many of the Gs-associated signaling components reside on the cytoplasmic leaflet of the erythrocyte plasma membrane, rendering them inaccessible to most extracellular probes. Since erythrocytes are enucleated and terminally differentiated, they cannot be transfected to express exogenous transgenes. We have modified methods of hypotonic lysis and isotonic resealing to generate loaded erythrocyte ghosts that can be efficiently infected by Plasmodium falciparum and sustain normal levels of intraerythrocytic parasite growth and replication. Further, we show that these ghosts can be filled with various membrane-impermeable peptides or other proteinaceous cargoes for studying signaling and transport events inside the erythrocyte. Resealed ghosts morphologically resemble normal erythrocytes, albeit with reduced hemoglobin content. Other measures of erythrocyte function and malarial infection are being investigated. Studies will be presented on the use of ‘reconstituted’ erythrocytes in elucidating mechanisms parasite invasion as well as parasite protein trafficking in erythrocytes infected by P. falciparum.
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Okoyeh, Jude Nnaemeka, C. R. Pillai, and Chetan E. Chitnis. "Plasmodium falciparum Field Isolates Commonly Use Erythrocyte Invasion Pathways That Are Independent of Sialic Acid Residues of Glycophorin A." Infection and Immunity 67, no. 11 (November 1, 1999): 5784–91. http://dx.doi.org/10.1128/iai.67.11.5784-5791.1999.
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ABSTRACT Erythrocyte invasion by malaria parasites is mediated by specific molecular interactions. Sialic acid residues of glycophorin A are used as invasion receptors by Plasmodium falciparum. In vitro invasion studies have demonstrated that some cloned P. falciparum lines can use alternate receptors independent of sialic acid residues of glycophorin A. It is not known if invasion by alternate pathways occurs commonly in the field. In this study, we used in vitro growth assays and erythrocyte invasion assays to determine the invasion phenotypes of 15 P. falciparum field isolates. Of the 15 field isolates tested, 5 multiply in both neuraminidase and trypsin-treated erythrocytes, 3 multiply in neuraminidase-treated but not trypsin-treated erythrocytes, and 4 multiply in trypsin-treated but not neuraminidase-treated erythrocytes; 12 of the 15 field isolates tested use alternate invasion pathways that are not dependent on sialic acid residues of glycophorin A. Alternate invasion pathways are thus commonly used by P. falciparum field isolates. Typing based on two polymorphic markers, MSP-1 and MSP-2, and two microsatellite markers suggests that only 1 of the 15 field isolates tested contains multiple parasite genotypes. Individual P. falciparum lines can thus use multiple invasion pathways in the field. These observations have important implications for malaria vaccine development efforts based on EBA-175, the P. falciparumprotein that binds sialic acid residues of glycophorin A during invasion. It may be necessary to target parasite ligands responsible for the alternate invasion pathways in addition to EBA-175 to effectively block erythrocyte invasion by P. falciparum.
Dissertations / Theses on the topic "Erythrocytes invasion"
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Jones, Matthew L. "Erythrocyte invasion by Plasmodium falciparum." Thesis, Birmingham, Ala. : University of Alabama at Birmingham, 2009. https://www.mhsl.uab.edu/dt/2009r/jonesm.pdf.
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Scheetz, Emily. "Erythrocyte Biology and its Impact on Plasmodium vivax Invasion." Cleveland, Ohio : Case Western Reserve University, 2008. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=case1216148822.
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Dankwa, Selasi. "Sialic acid variation as a determinant of Plasmodium invasion of erythrocytes in malaria infection." Thesis, Harvard University, 2015. http://nrs.harvard.edu/urn-3:HUL.InstRepos:17467188.
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Sialic acids are acidic sugars that terminate glycan chains on proteins or lipids on vertebrate cell surfaces. They vary greatly in structure, presentation and amount, all of which are important physiologically, but can also impact the tissue and host tropism of diverse pathogens.
Parasites of the genus Plasmodium cause malaria, a disease characterized by a cyclical process of parasite invasion of host erythrocytes, growth and replication and fresh invasion of new erythrocytes. During erythrocyte invasion – an event central to malaria pathogenesis – proteins on the surface of the parasite, known as invasion ligands, bind to specific erythrocyte receptors, many of which are sialylated. In this dissertation, we determined how sialic acid variation impacts erythrocyte invasion by the zoonotic parasite, Plasmodium knowlesi and the most virulent human parasite, Plasmodium falciparum.
For studies on P. knowlesi, we determined if Neu5Gc, a sialic acid that is absent in humans but present in most other primates, is a major determinant of parasite tropism. We used the recently described ex vivo erythrocyte culture system to transgenically express the CMAH enzyme, responsible for production of Neu5Gc. P. knowlesi showed significantly increased invasion of Neu5Gc-expressing human erythrocytes, providing evidence that loss of Neu5Gc in humans restricts P. knowlesi invasion of human erythrocytes. We then biochemically characterized two P. knowlesi invasion ligands of the EBL family and found they specifically bind Neu5Gc. These ligands potentially mediate Neu5Gc-dependent invasion of human and macaque erythrocytes. We finally showed that in natural human infections, P. knowlesi can adapt to infect erythrocytes independently of sialic acid.
We also studied the use of sialic acid-containing erythrocyte receptors by P. falciparum using the ex vivo erythrocyte culture system. We determined the importance in invasion of glycophorin B (GPB), receptor for P. falciparum invasion ligand, EBL-1, and one of the highly sialylated receptors on the erythrocyte surface. We specifically knocked down gene expression of GPB as well as two well characterized receptors involved in P. falciparum invasion – GPA, the largest contributor to erythrocyte sialic acid and GPC, another sialylated receptor. Invasion assays using P. falciparum laboratory strains and field isolates revealed that GPB is a dominant receptor in P. falciparum invasion, of comparable importance to GPA.Biological Sciences in Public Health
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Tetteh-Quarcoo, Patience Borkor. "Investigations into polymorphisms within complement receptor type 1 (CD35) thought to protect against severe malaria." Thesis, University of Edinburgh, 2012. http://hdl.handle.net/1842/6193.
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The human immune-regulatory protein, complement receptor type 1 (CR1, CD35), occurs on erythrocytes where it serves as the immune adherence receptor. It interacts with C3b, C4b, C1q and mannan-binding lectin (MBL). It additionally binds the Plasmodium falciparum protein, Rh4, in the non-sialic acid-dependent erythrocye-invasion pathway, and is also important for rosetting, via an interaction with P. falciparum erythrocyte membrane protein 1 (PfEMP1). A C3b/C4b, and PfEMP1 binding site lies in CCP modules 15-17 (out of 30 in CR1), while polymorphisms that afford advantage to some populations in dealing with severe malaria occur in CCPs 24-25, begging the question central to this thesis – do these polymorphism modulate function, and if so how? We hypothesized that the CR1 architecture apposes CCPs 15-17 and CCPs 24-25 using the exceptionally long linker between CCPs 21 and 22 as a hinge, thus polymorphic variants in CCPs 24-25 modulate functionality in CCPs 15-17. To test this, a panel of recombinant CR1 protein fragments (CCPs 21, 21-22, 20-23, 15-17, 17, 10-11, 17-25, 15-25 and 24-25) were produced in Pichia pastoris along with polymorphic forms of the relevant constructs. After purification, biophysical and biological methods were used to assess whether the linker does indeed act as a hinge, and the comparative abilities of the CCPs 15-25 variants (along with soluble CR1 (sCR1), CCPs 1-3 and the panel of CR1 fragments) to interact with a range of ligands were measured. We found no evidence from NMR for face-to-face contacts between CCPs 21 and 22 that would be consistent with the long linker permitting a 180-degree bend between them. Indeed, based on scattering and analytical ultracentrifugation data, CCPs 20-23 form an extended rather than a bent-back structure. All of the four Knops blood-group variants of the CCPs 15-25 proteins produced similar results according to dynamic light scattering and AUC indicating no structural difference or change in self-association state between variants. In addition, based on the data collected from surface plasmon resonance (SPR), ELISA and fluid-phase cofactor (for factor I) assays, there were no evidence of any difference between the polymorphic forms with respect to their interactions with C3b, C4b, C1q and MBL. Only weak interaction was observed for sCR1, and all CCPs 15-25 variants, with the relevant part of PfEMP1, and there was no measurable difference amongst the variants in disrupting rosettes. The sCR1-Rh4.9 interaction was confirmed by SPR; affinities measured between the binding domain of Rh4 and the panel of CR1 fragments identified CCPs 1-3 (site 1) as the main interaction site. It seemed unlikely therefore that CCPs 24 and 25 could modulate Rh4 binding; indeed none of the four CR1 15-25 variants bound Rh4.9 appreciably. Thus we concluded that allotypic variations in CCPs 24-25 have no measurable effect on the architecture as well as binding of CR1 to its host or parasite ligands The inferred selective pressure acting on these variants likely arise from some other (i.e. besides malaria) geographically localised infectious diseases.
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Hastings, C. H. "Novel malaria parasite proteins involved in erythrocyte invasion." Thesis, University College London (University of London), 2012. http://discovery.ucl.ac.uk/1380118/.
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Erythrocyte invasion is a key step in the Plasmodium life cycle. This process is tightly regulated, involving the sequential release of specialised apical secretory organelles – the micronemes, rhoptries and dense granules. These organelles contain proteins required for invasion and establishment of the parasitophorous vacuole, but most of the proteins remain uncharacterised. The aim of this project was to uncover novel proteins with a role in invasion by the human malaria parasite Plasmodium falciparum merozoites. I identified proteins using the following selection criteria: a) expression in the schizont/merozoite form of the parasite; b) conservation across the genus; c) the presence of a signal peptide and d) one or more transmembrane (TM) domains. A list of 64 proteins was identified, and filtered further based on novelty, presence in the merozoite proteome, expression in other life cycle stages, and difficulty of study. Five proteins were selected, and I produced recombinant protein and raised antibodies against three, which I used to identify the sub-cellular location of the protein within the parasite. The proteins appear to reside in either the rhoptries or the endoplasmic reticulum of the merozoite. Attempts were made to epitope-tag and delete all 3 genes, with a focus on one protein, the type IV Hsp40, PF11_0443. This protein contains two TM domains and is expressed during schizogony. By immunofluorescence it is present in the ER of early schizonts, before accumulating at the apex of merozoites in a rhoptry location. Immunoprecipitation experiments indicated that the protein binds known rhoptry proteins and other chaperones. The protein has been epitope-tagged but attempts to delete the gene by genetic recombination were unsuccessful. The gene is conserved in Plasmodium spp. and there are orthologues in higher eukaryotes, but it is absent from other Apicomplexa. Current studies are focused on the role of this protein in erythrocyte invasion.
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Bera, Sagorika. "Analysis of Antibody-Induced Plasmodium falciparum Sporozoites Through Scanning Electron Microscopy." Scholar Commons, 2017. http://scholarcommons.usf.edu/etd/6679.
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Malaria is a devastating disease that continues to affect millions of people worldwide every year. Specifically, Plasmodium falciparum is the most common human malaria parasite, particularly in sub-Saharan Africa. P. falciparum causes the most malignant and debilitating symptoms with the highest mortality and complication rates. Even with the worldwide efforts of many researchers and organizations, the road to discovering a vaccine has been difficult and challenging. Due do to the improvements in in vitro liver stage assays as well as rodent models of mammalian malaria, pre-erythrocytic stages of malaria have become a more accessible target for experimental studies. These vaccine candidates target Plasmodium sporozoites in the liver and liver stages to prevent development to the blood-stage forms, which is responsible for the debilitating symptoms of the disease. Scanning electron microscopy has been used for decades to provide insight on the morphology and topography of specimens, which cannot be seen through a light microscope. The purpose of this study was to analyze the morphology of sporozoites with some target antibodies. Sporozoites have previously shown uncharacterized appearances and development in an immunofluorescent stain at different concentrations of particular antibodies. With this further understanding on the morphological impact few of the target antibodies have on sporozoites through scanning electron microscopy, further grasp can be acquired.
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Alghamdi, Sultan Ahmed. "Genetic determinants of selectivity of erythrocyte invasion in the human malaria parasite Plasmodium falciparum." Thesis, University of Glasgow, 2015. http://theses.gla.ac.uk/6605/.
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The aim of this study was to investigate the genetic basis of selectivity in invasion of the red blood cells by the human malaria parasite Plasmodium falciparum. Multiple invasions of a single host red blood cell by more than one merozoite, which can be described or assessed in terms of the selectivity index (SI), has been reported to be related to the severity of malaria disease. In this study, selectivity index, defined as the ratio of the number of multiply-infected red cells observed to that expected from random invasion, as modelled by a Poisson distribution was determined for certain clones of P.falciparum. SI was measured under static and shaking culturing conditions for P. falciparum clones 3D7 and HB3 and 18 progeny clones derived from a genetic cross between these two parasite clones. P. falciparum clone 3D7 was found to have a significantly lower SI than HB3 under both static and shaking culture conditions. There was no relationship between SI and days in continuous culture for clone 3D7 under shaking and static conditions; the phenotype therefore appears to be stable over time. The genetic basis of the difference in selectivity index between P. falciparum clones 3D7 and HB3 was investigated in progeny clones from a cross between these two clones, to ascertain the inheritance pattern of the phenotype. Under static conditions, ten progeny clones had a selectivity index lower than either parent, one progeny clone had higher selectivity index than both parent, and six progeny clones had selectivity index intermediate between the parents . Under shaking conditions, fifteen progeny clones were observed to have a selectivity index lower than either parent. These observations suggest the involvement of more than one parasite gene in selectivity index. A Quantitative Trait Locus (QTL) analysis was performed in order to identify genomic regions influencing SI in the progeny clones. The highest LOD score of 5.06 was obtained for a QTL on chromosome 13 for SI measured in parasites cultured under shaking conditions. This QTL denoted, PF_SI_1, extends for approximately 100kb on chromosome 13 and contains 19 open reading frames. This finding indicates the presence of a gene or genes on chromosome 13 that influence the parasite’s selection of erythrocytes for invasion.
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Downing, Sarita Louise. "Characterization of Plasmodium falciparum merozoite apical membrane antigen-1 protein changes prior to erythrocyte invasion." Diss., University of Pretoria, 2016. http://hdl.handle.net/2263/61680.
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Malaria is a global pandemic that affects millions of people each year. It is a parasitic
infection caused by the Plasmodium family, with Plasmodium falciparum being the most
virulent strain. Malaria is transmitted to humans by the female Anopheles mosquito. The
parasite undergoes two different cycles of its life cycle within the human host: the liver
and intraerythrocytic life cycle. The latter consists of an asexual and sexual cycle. The
intraerythrocytic cycle is perhaps the most important stage of the parasite's life cycle as it
promotes the spread of the disease within and between hosts. The focus of this
investigation was aimed at the invasion process of the merozoites into the erythrocytes.
The Plasmodium merozoite utilises a cascade of proteins during the erythrocyte invasion
process, which is a swift action that takes place in approximately 30 seconds. A number
of surface proteins are expressed during merozoite development and are distributed along
the merozoite surfaces to assist with attachment and invasion, the most crucial being
MSP-1, AMA-1 and RON-2. MSP-1 and AMA-1 are vital targets for the development of
malaria vaccines.
AMA-1 is the central target protein of this investigation as it plays an essential role in the
invasion process. AMA-1 commits the merozoite to invade the erythrocyte, as it assists
the RON proteins in the formation of an irreversible tight-junction with the membrane of
the erythrocyte. Antibodies, specific to AMA-1, bind to the protein, which prevents the
formation of the tight junction and inhibits the invasion of the merozoite into the
erythrocyte, therefore preventing the spread of the disease.
However, before invasion, AMA-1 undergoes a number of proteolytic processes. It is
synthesized as an 83 kDa (AMA-183) precursor protein in the apical organelle of the
merozoite. This is then cleaved at the N-terminus to give rise to a 66 kDa (AMA-166)
fragment, which is secreted onto the surface of the merozoite. The AMA-166 fragment is
then cleaved into either a 48 kDa (AMA-148) or 44 kDa (AMA-144) fragment. One of
these three fragments is then used by the merozoite for erythrocyte invasion.
The aim of this investigation was to isolate and characterise each of the fragments of the
Plasmodium falciparum AMA-1 (PfAMA-1) protein using the 3D7 lab strain of P. falciparum and to visualise the merozoite-erythrocyte invasion process, to possibly
identify which of the AMA-1 fragments are involved in the invasion process. In order to
achieve this large clusters of merozoites from sorbitol-synchronised cultures were
isolated. Schizonts were isolated from culture by magnetic separation and incubated with
E64 to prevent the release of merozoites. Merozoites that were required for the isolation
of PfAMA-1 were harvested from the schizonts by saponin lysis, then homogenised,
separated by SDS-PAGE and digested for LC-MS/MS analysis. Merozoites that were
required for the visualisation procedures were not incubated with E64, to allow natural
egression from the erythrocyte.
The transmission electron microscopy results produced clear images of the merozoiteerythrocyte
invasion process and the positioning of PfAMA-1 on the merozoite, before
and after schizont rupture, was visualised from results obtained from confocal
microscopy. Then PfAMA-1 was identified in isolated merozoite samples by LC-MS/MS
analysis. However, due to its low abundance, isolation of high enough concentrations of
PfAMA-1 to characterise its different fragments was not achieved.
Further investigation into the development of the culturing and isolating methods could
help in future projects aimed at isolating higher concentrations of merozoite proteins
from synchronised cultures with a lower merozoite egression window period, in order to
accomplish detailed analysis on invading proteins for the future development of
treatments against malaria.Dissertation (MSc)--University of Pretoria, 2016.
Pharmacology
MSc
Unrestricted
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Rees-Channer, Roxanne. "Motoring merozoites : the role of gliding-associated proteins GAP45 and GAP50 in erythrocytic invasion." Thesis, University College London (University of London), 2009. http://discovery.ucl.ac.uk/15937/.
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A conserved acto-myosin motor complex is implicated in parasite motility and host invasion by a wide variety of Apicomplexan zoites. Until recently, only actin, myosin A (MyoA) and its putative light chain (MLC1 in Toxoplasma gondii) or myosin tail domain interacting protein (MTIP) in Plasmodium spp., had been identified as central to the function of this motor. Identification of two further components in T. gondii, the gliding-associated proteins (GAP45 and GAP50), has provided a valuable insight into how the motor may be anchored in the inner membrane complex (IMC) that lies below the plasma membrane. Results presented here demonstrate that Plasmodium falciparum (Pf)GAP45 and PfGAP50 are expressed and co-localise with PfMTIP at the periphery of merozoites. Both GAPs are found to be in complex with PfMyoA, and PfMTIP. Pulse-chase experiments indicate that the motor complex is assembled in two stages. PfGAP50 is incorporated after the formation of a ternary complex comprising PfGAP45, PfMyoA and PfMTIP. PfGAP45 is shown to be N-myristoylated and palmitoylated and may therefore function as a linker protein tethering the motor to the outer leaflet of IMC. Additionally, PfGAP45 is phosphorylated by calmodulin-dependent protein kinase 1 (CDPK1); a process that may be important in the regulation of the motor. Recombinant PfGAP50 is a well-ordered protein, whereas PfGAP45 has a low content of secondary structure. Potential interaction of GAPs with other motor components has been examined. Co-immunoprecipitation experiments, circular dichroism (CD) and fluorescence spectroscopic analyses have not provided any evidence of direct interaction with any other motor proteins.
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Baron, Kim L. "Enzymatic and chemical modifications of erythrocyte surface antigens to identify Plasmodium falciparum merozoite binding sites." Diss., University of Pretoria, 2014. http://hdl.handle.net/2263/46043.
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Malaria is a disease caused by the protozoan parasite Plasmodium where the species that causes the most severe form of malaria in humans is known as Plasmodium falciparum. At least 40% of the global population is at risk of contracting malaria with 627 000 people dying as a result of this disease in 2012. Approximately 90% of all malaria deaths occur in sub-Saharan Africa, where approximately every 30 seconds a young child dies, making malaria the leading cause of death in children under the age of five years old.
The malaria parasite has a complex life cycle utilising both invertebrate and vertebrate hosts across sexual and asexual stages. The erythrocyte invasion stage of the life cycle in the human whereby the invasive merozoite form of the parasite enters the erythrocyte is a central and essential step, and it is during this stage that the clinical symptoms of malaria manifest themselves. Merozoites invade erythrocytes utilising multiple, highly specific receptor-ligand interactions in a series of co-ordinated events. The aim of this study was to better understand the interactions occurring between the merozoite and erythrocyte during invasion by using modern, cutting-edge proteomic techniques. This was done in the hope of laying the foundation for the discovery of new key therapeutic targets for antimalarial drug and vaccine-based strategies, as there is currently no commercially available antimalarial vaccine and no drug to which the parasite has not at least started showing resistance.
In this study healthy human erythrocytes were treated separately with different protein-altering enzymes and chemicals being trypsin, the potent oxidant sodium periodate (NaIO4), the amine cross-linker tris(2-chloroethyl)amine hydrochloride (TCEA) and the thiol cross-linker 1,11-bis(maleimido)triethylene glycol (BM(PEG)3). The resulting erythrocyte protein alterations were visualised as protein band differences on sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS PAGE), where treated and untreated control erythrocyte ghost protein fingerprints were visually compared to one another. The protein bands showing differences between treated and control samples were in-gel digested using trypsin then sequenced by liquid chromatography tandem mass spectrometry (LC-MS/MS) and identified using proteomics-based software. In this way, the erythrocyte proteins altered by each enzyme/chemical treatment were identified.
Malaria invasion assays were performed where each treatment group of erythrocytes as well as the control erythrocytes were incubated separately with schizont stage malaria parasites for the duration of one complete life cycle. Using fluorescent staining and flow cytometry, the invasion inhibition efficiency for each treatment group was evaluated. By utilising these methods, the identification and the relative importance of the erythrocyte proteins involved in the invasion process were determined. Protein fingerprints of control and treated erythrocyte ghosts were visualised and optimised on SDS PAGE where induced protein band differences were successfully identified by LC-MS/MS. It was found that each treatment altered erythrocyte proteins with changes found in Band 3, actin, phosphoglycerate kinase 1, spectrin alpha, spectrin beta, ankyrin, haemoglobin, Bands 4.1 and 4.2, glycophorin A and stomatin. The invasion assays revealed that TCEA inhibited invasion to the greatest extent as compared to the other treatments, followed by BM(PEG)3 and trypsin. Sodium periodate-treated erythrocytes could not be assessed using the invasion assay due to auto-haemolysis. Band 3, glycophorin A, Band 4.1 and stomatin appear to be of higher relative importance in the invasion process as compared to the other altered erythrocyte proteins. These results confirmed the known roles of spectrin alpha, spectrin beta, glycophorin A, Band 3 and Band 4.1 in invasion, and suggested that ankyrin, Band 4.2 and stomatin may also be involved.
This study highlighted the potential that modern, cutting-edge proteomic techniques provide when applied to previous comparative studies found in older literature, as previously unidentified proteins that can be involved in invasion were revealed.
These results can be used as a foundation in future studies in order to identify new key targets for the development of new antimalarial drug- and vaccine-based strategies, with the hope of preventing the suffering of the millions of malaria-inflicted people worldwide, and ultimately eradicating this deadly disease.Dissertation (MSc)--University of Pretoria, 2014.
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Books on the topic "Erythrocytes invasion"
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Roth, Stephen Joel. The effect of anti-glycophorin A monoclonal antibodies and FAB fragments on Plasmodium falciparum erythrocyte invasion in vitro. [New Haven: s.n.], 1986.
Find full textBook chapters on the topic "Erythrocytes invasion"
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Hadley, Terence J., and Louis H. Miller. "Invasion of Erythrocytes by Malaria Parasites: Erythrocyte Ligands and Parasite Receptors." In Chemical Immunology and Allergy, 49–71. Basel: KARGER, 1988. http://dx.doi.org/10.1159/000318613.
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Howard, Russell J., and Louis H. Miller. "Invasion of Erythrocytes by Malaria Merozoites: Evidence for Specific Receptors Involved in Attachment and Entry." In Ciba Foundation Symposium 80 - Adhesion and Microorganism Pathogenicity, 202–19. Chichester, UK: John Wiley & Sons, Ltd., 2008. http://dx.doi.org/10.1002/9780470720639.ch13.
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Gaur, Deepak, Chetan E. Chitnis, and Virander S. Chauhan. "Molecular basis of erythrocyte invasion byPlasmodiummerozoites." In Advances in Malaria Research, 33–86. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2016. http://dx.doi.org/10.1002/9781118493816.ch3.
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Riglar, David T., and Jake Baum. "Static and Dynamic Imaging of Erythrocyte Invasion and Early Intra-erythrocytic Development in Plasmodium falciparum." In Methods in Molecular Biology, 269–80. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-62703-026-7_18.
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Bei, Amy Kristine, and Manoj T. Duraisingh. "Measuring Plasmodium falciparum Erythrocyte Invasion Phenotypes Using Flow Cytometry." In Malaria Vaccines, 167–86. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4939-2815-6_14.
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Aikawa, Masamichi, and Louis H. Miller. "Structural Alteration of the Erythrocyte Membrane During Malarial Parasite Invasion and Intraerythrocytic Development." In Novartis Foundation Symposia, 45–63. Chichester, UK: John Wiley & Sons, Ltd., 2008. http://dx.doi.org/10.1002/9780470715444.ch4.
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Sherman, Irwin W. "Chapter 23 Invasion of Erythrocytes." In Reflections on a Century of Malaria Biochemistry, 229–52. Elsevier, 2008. http://dx.doi.org/10.1016/s0065-308x(08)00423-5.
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Joshi, Urja, Dhara Jani, Linz-Bouy George, and Hyacinth Highland. "Antioxidant Efficacy of Selected Plant Extracts Debilitates the Plasmodium Invasion through Erythrocytic Membrane Stabilisation - An In Vitro Study." In Malaria - Recent Advances, and New Perspectives [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.106844.
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Most dangerous and prevalent form of malaria is caused by the Plasmodium falciparum mediated malaria and poses the greatest threat to the humans. Emergence of multi drug resistant parasite hindered the prevention of malaria burden worldwide. This study is mainly focused on the erythrocytic membrane stabilisation using regionally available medicinal plant extracts and its corelation with the oxidative stress generated during the intracellular erythrocytic stages development of Plasmodia. The results disclosed that antioxidant potential of the medicinal plants can diminish the reactive oxygen species generation leads to restrict the plasmodial invasion into erythrocytes ultimately decreases the parasitic load. Hence, the evidence of the effective phytochemicals present in the selected medicinal plants can be the promising anti-plasmodial drug candidates as a future perspective.
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Akunwata, Chima. "Duffy Antigens and Malaria: The African Experience." In Blood Groups - More than Inheritance of Antigenic Substances. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.102014.
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The Duffy blood group antigen is also known as Duffy Antigen Receptor for Chemokines (DARC) serves more functions than just a blood group antigen for serological reactions. It is a receptor for pro-inflammatory chemokines and Plasmodium vivax invasion of the red blood cells. A point mutation in the promoter region of the Duffy gene disrupts the binding of a transcription factor, leading to a lack of expression of the antigen on the erythrocytes. This Duffy negative phenotype is found predominantly in the African population. This mutation is advantageous as individuals with the Fy(a-b-) phenotype are less susceptible to P. vivax malaria. Malaria is caused by plasmodium parasites and it is endemic in Africa, where it is one of the leading causes of morbidity and mortality. It is believed that the absence of Duffy antigen in most Africans contributed to the resistance to P. vivax and by extension, reduced the burden of malaria in these endemic areas.
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"Invasive Asian Carps in North America." In Invasive Asian Carps in North America, edited by Diana M. Papoulias, James Candrl, Jill A. Jenkins, and Donald E. Tillitt. American Fisheries Society, 2011. http://dx.doi.org/10.47886/9781934874233.ch18.
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<em>Abstract</em>.—The Asian black carp <em>Mylopharyngodon piceus </em>is of interest to the aquaculture industry in the United States as a biological control for snails and mollusks. However, past experience in North America with other Asian carps has raised concern that black carp will establish wild populations and negatively affect native populations of fish and invertebrates, especially mollusks. The demand for black carp has led biologists to seek ways to allow their use while at the same time maintaining control over their distribution and reproduction. Physical containment and restrictions on importation, release, and stocking have mostly failed. Control of reproduction holds more promise. The induction of triploidy (having three sets of chromosomes), which can render an individual biologically sterile, is of particular interest. The main purpose of this study was to evaluate the efficiency of proposed testing procedures used to assure genetic triploidy in black carp prior to distribution by the state of Missouri, using black carp and grass carp <em>Ctenopharyngodon idella</em>. Our objectives were to (1) verify if the ploidy determination methodology (nuclear size) employed was 100% accurate, (2) determine growth and survival of juvenile black carp over extended periods of time under laboratory and pond conditions, and (3) histologically examine development and gametogenesis in gonads collected from triploid and diploid black and grass carps of different ages and stages of maturation. Comparison of erythrocyte nuclear size using the Coulter counter method versus the more accurate method of flow cytometry that measures DNA content indicated an error rate of 0.25% by the former method. Black carp grew and survived well in mid-Missouri ponds. Triploid grass carp males appeared to produce functional gametes, and some triploid black carp male testes had apparently normal spermatocytes within cysts. A few normally developing oocytes at previtellogenic and vitellogenic stages were observed in triploid grass carp females, and a few normal perinuclear oocytes could be identified in triploid black carp females. Currently, the standards of the U.S. Fish and Wildlife Service’s triploid grass carp voluntary inspection program are being followed by some states to manage triploid black carp. Our results indicate that although the percentage of diploid black carp that could pass through the currently proposed screening program is small, overall numbers of diploid black carp distributed in a state could be substantial depending on the number of triploids distributed. Furthermore, despite indications that triploid male black carp can be expected to be functionally sterile, reproductive studies may be warranted given the large wild populations of diploid grass carp, bighead carp <em>Hypophthalmichthys nobilis</em>, and silver carp <em>H. molitrix </em>in the Mississippi River basin system.
Conference papers on the topic "Erythrocytes invasion"
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Rusu, Stefan. "Establishing of the mono- and polyinvasion impact on some morpho-functional indices in wild boars." In Xth International Conference of Zoologists. Institute of Zoology, Republic of Moldova, 2021. http://dx.doi.org/10.53937/icz10.2021.44.
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In the paper is described the mono- and poly-invasions impact on some morpho-functional indices in wild boars. So, in result of the investigation of hematological indices in uninfested mono- and poly-parasitized wild boars, it was established that both the indices of hemoglobin content, of hematocrit, erythrocyte’s number, thrombosis time and ESR (erythrocyte sedimentation rate) vary and are more increased in the I group with uninfested wild boars compared to mono - and poly-parasitized ones. It has been established that at infested boars with S. papillosus from the I group, and in those infested with D. lanceolatum from the II group there is a decrease of hemostatic indices, but their maximum decrease is highlighted in the IV group with wild boars infested with Dicrocoelium lanceolatum, Strongyloides papillosus, Metastrongylus elongatus and Eimeria debliecki. This decrease is due to eliminated exotoxins by parasites, which contain anticoagulants and hemolyzers and which neutralize the fibrinogen, thrombin, Ca+ ions and vitamin K properties from the body.
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Yamamoto, Hidetake. "Development of Minimal Invasive SMA Multi-Transducer Unit for Blood Analysis or Drug Delivery." In ASME 2010 5th Frontiers in Biomedical Devices Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/biomed2010-32008.
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This research purpose is to develop minimal medical units applying heated actuations of the Shape Memory Alloy (SMA) transducers using the medical Ti-Ni material, in order to enable minimal hypodermic invasive microvolume either blood suction or drug delivery by equipping nontoxic and minimal edged microneedle to be created in my laboratory. I have focused on lymphocytes for immunotoxin and erythrocytes for glucose level in blood. This paper has reported double-action mechanisms of the compact unit in originally developing and its actions by low DC inputs. The Joule’s heating of the SMA coil spring transducer might be useful for indenting blood vessels whose diameter was larger than the microneedle because of generating indentation stroke of 2 mm and recovery force of 0.25 N 0.6 s later from heating when applied DC 2 V and 0.5 A. When applied DC 1.5 V and 2 A, the octagonal-pyramidal foil transducer for blood suction recovered as plane condition as before octagonal-pyramidal forming 8 s later from heating.