scholarly journals Light microscopic detection of Plasmodium falciparum in vitro through Pf histidine rich protein 2 (HRP 2) gold conjugate labeling: Rapid diagnosis of cerebral malaria in humans

2014 ◽  
Vol 13 (8) ◽  
pp. 978-982
Author(s):  
Olalekan Michael Ogundele ◽  
Sabiu Saheed ◽  
Adeshina Oloruntoba Adekeye ◽  
Philip Adeyemi Adeniyi ◽  
Oluwatosin Olalekan Ogedengbe ◽  
...  
Keyword(s):  
Plasmodium Falciparum ◽  
Cerebral Malaria ◽  
Rapid Diagnosis ◽  
Microscopic Detection ◽  
Gold Conjugate

In vitro antimalarial activity and molecular modeling studies of novel artemisinin derivatives

RSC Advances ◽  
2015 ◽  
Vol 5 (59) ◽  
pp. 47959-47974 ◽  
Author(s):  
Rashmi Gaur ◽  
Harveer Singh Cheema ◽  
Yogesh Kumar ◽  
Suriya Pratap Singh ◽  
Dharmendra K. Yadav ◽  
...  
Keyword(s):  
Plasmodium Falciparum ◽  
Molecular Modeling ◽  
Cerebral Malaria ◽  
Antimalarial Activity ◽  
Anopheles Mosquito ◽  
Fatal Disease ◽  
Artemisinin Derivatives ◽  
Modeling Studies ◽  
Molecular Modeling Studies

Cerebral malaria is a serious and sometimes fatal disease caused by aPlasmodium falciparumparasite that infects a female anopheles mosquito which feeds on humans.

scholarly journals Plasmodium falciparum-infected erythrocyte receptor(s) for CD36 and thrombospondin are restricted to knobs on the erythrocyte surface.

1992 ◽  
Vol 40 (9) ◽  
pp. 1419-1422 ◽  
Author(s):  
K Nakamura ◽  
T Hasler ◽  
K Morehead ◽  
R J Howard ◽  
M Aikawa
Keyword(s):  
Endothelial Cells ◽  
Plasmodium Falciparum ◽  
Cerebral Malaria ◽  
Vascular Occlusion ◽  
Cerebral Microvessels ◽  
Erythrocyte Surface ◽  
Infected Rbcs ◽  
First Time

Adherence of Plasmodium falciparum-infected RBCs (PRBC) to endothelial cells causes PRBC sequestration in cerebral microvessels and is considered to be a major contributor to the pathogenesis of cerebral malaria. Both CD36 and thrombospondin (TSP) are glycoproteins that mediate PRBC adherence to endothelial cells in vitro. Because they are both expressed on the surface of endothelial cells, they probably contribute to PRBC sequestration and vascular occlusion in vivo. By applying affinity labeling of receptor binding sites with purified ligands, we showed for the first time that both CD36 and TSP can bind independently to the PRBC surface and that the PRBC receptor(s) for CD36 and TSP are localized specifically to the electron-dense knob protrusions of the PRBC surface. These findings may help in efforts to develop a malaria vaccine to prevent cerebral malaria.

scholarly journals KOMUNIKASI PENDEK Perbanyakan Tanaman Artemisia annua secara In Vitro

2016 ◽  
Vol 4 (1) ◽  
pp. 41
Author(s):  
Rossa Yunita ◽  
Endang G. Lestari
Keyword(s):  
Plasmodium Falciparum ◽  
Cerebral Malaria ◽  
In Vitro Propagation ◽  
Artemisia Annua ◽  
Ms Medium ◽  
Marked Activity ◽  
Good For

<p>Artemisinin, an anti-malarial medicine<br />isolated from the annual wormwood Artemisia annua,<br />has a marked activity against chloroquine-resistant and<br />chloroquine-sensitive strains of Plasmodium falciparum.<br />This compound is useful for treatment of cerebral malaria.<br />An in vitro propagation system for A. annua has been developed.<br />Shoots were induced by culturing seeds of A.<br />annua on a MS medium containing BAP (0, 0.1, 0.3, 0.5<br />mg/l). Shoots were also formed on each seedling cultured<br />on the same medium. Root formations were obtained from<br />shoots that were subcultured on a MS medium containing<br />IBA (0, 1.0, 1.5, 2 mg/l). The results showed that MS medium<br />supplemented with BAP 0.3 mg/l was the best medium for<br />induction and multiplication of the shoots, while the MS<br />medium supplemented with IBA (1 mg/l) was good for root<br />formations.</p>

scholarly journals Natural and Vaccine-Induced Acquisition of Cross-Reactive IgG-Inhibiting ICAM-1-Specific Binding of a Plasmodium falciparum PfEMP1 Subtype Associated Specifically with Cerebral Malaria

2018 ◽  
Vol 86 (4) ◽  
Author(s):  
Rebecca W. Olsen ◽  
Gertrude Ecklu-Mensah ◽  
Anja Bengtsson ◽  
Michael F. Ofori ◽  
John P. A. Lusingu ◽  
...  
Keyword(s):  
Plasmodium Falciparum ◽  
Cerebral Malaria ◽  
Specific Binding ◽  
Intercellular Adhesion Molecule ◽  
Enzyme Linked Immunosorbent Assay ◽  
Intercellular Adhesion Molecule 1 ◽  
Content Type ◽  
Protein Receptor ◽  
Specific Igg

ABSTRACT Cerebral malaria (CM) is a potentially deadly outcome of Plasmodium falciparum malaria that is precipitated by sequestration of infected erythrocytes (IEs) in the brain. The adhesion of IEs to brain endothelial cells is mediated by a subtype of parasite-encoded erythrocyte membrane protein 1 (PfEMP1) that facilitates dual binding to host intercellular adhesion molecule 1 (ICAM-1) and endothelial protein receptor C (EPCR). The PfEMP1 subtype is characterized by the presence of a particular motif (DBLβ_motif) in the constituent ICAM-1-binding DBLβ domain. The rate of natural acquisition of DBLβ_motif-specific IgG antibodies and the ability to induce such antibodies by vaccination are unknown, and the aim of this study was to provide such data. We used an enzyme-linked immunosorbent assay (ELISA) to measure DBLβ-specific IgG in plasma from Ghanaian children with malaria. The ability of human immune plasma and DBLβ-specific rat antisera to inhibit the interaction between ICAM-1 and DBLβ was assessed using ELISA and in vitro assays of IE adhesion under flow. The acquisition of DBLβ_motif-specific IgG coincided with age-specific susceptibility to CM. Broadly cross-reactive antibodies inhibiting the interaction between ICAM-1 and DBLβ_motif domains were detectable in immune plasma and in sera of rats immunized with specific DBLβ_motif antigens. Importantly, antibodies against the DBLβ_motif inhibited ICAM-1-specific in vitro adhesion of erythrocytes infected by four of five P. falciparum isolates from cerebral malaria patients. We conclude that natural exposure to P. falciparum as well as immunization with specific DBLβ_motif antigens can induce cross-reactive antibodies that inhibit the interaction between ICAM-1 and a broad range of DBLβ_motif domains. These findings raise hope that a vaccine designed specifically to prevent CM is feasible.

Ultrastructural observations on the in vitro cytoadherence of Plasmodium falciparum infected red blood cells

1990 ◽  
Vol 48 (3) ◽  
pp. 914-915
Author(s):  
D.J.P. Ferguson ◽  
A.R. Berendt ◽  
J. Tansey ◽  
K. Marsh ◽  
C.I. Newbold
Keyword(s):  
Plasmodium Falciparum ◽  
Red Blood Cells ◽  
Blood Cells ◽  
Umbilical Vein ◽  
Cell Types ◽  
Amelanotic Melanoma ◽  
Cytoplasmic Process ◽  
Umbilical Vein Endothelial Cells

In human malaria, the most serious clinical manifestation is cerebral malaria (CM) due to infection with Plasmodium falciparum. The pathology of CM is thought to relate to the fact that red blood cells containing mature forms of the parasite (PRBC) cytoadhere or sequester to post capillary venules of various tissues including the brain. This in vivo phenomenon has been studied in vitro by examining the cytoadherence of PRBCs to various cell types and purified proteins. To date, three Ijiost receptor molecules have been identified; CD36, ICAM-1 and thrombospondin. The specific changes in the PRBC membrane which mediate cytoadherence are less well understood, but they include the sub-membranous deposition of electron-dense material resulting in surface deformations called knobs. Knobs were thought to be essential for cytoadherence, lput recent work has shown that certain knob-negative (K-) lines can cytoadhere. In the present study, we have used electron microscopy to re-examine the interactions between K+ PRBCs and both C32 amelanotic melanoma cells and human umbilical vein endothelial cells (HUVEC).We confirm previous data demonstrating that C32 cells possess numerous microvilli which adhere to the PRBC, mainly via the knobs (Fig. 1). In contrast, the HUVEC were relatively smooth and the PRBCs appeared partially flattened onto the cell surface (Fig. 2). Furthermore, many of the PRBCs exhibited an invagination of the limiting membrane in the attachment zone, often containing a cytoplasmic process from the endothelial cell (Fig. 2).

scholarly journals Stage-dependent effect of deferoxamine on growth of Plasmodium falciparum in vitro

Blood ◽  
1990 ◽  
Vol 76 (6) ◽  
pp. 1250-1255 ◽  
Author(s):  
S Whitehead ◽  
TE Peto
Keyword(s):  
Plasmodium Falciparum ◽  
Growth Inhibition ◽  
Antimalarial Activity ◽  
Clinical Malaria ◽  
Inhibitory Effect ◽  
Parasite Development ◽  
And Control ◽  
Speed Of Onset

Abstract Deferoxamine (DF) has antimalarial activity that can be demonstrated in vitro and in vivo. This study is designed to examine the speed of onset and stage dependency of growth inhibition by DF and to determine whether its antimalarial activity is cytostatic or cytocidal. Growth inhibition was assessed by suppression of hypoxanthine incorporation and differences in morphologic appearance between treated and control parasites. Using synchronized in vitro cultures of Plasmodium falciparum, growth inhibition by DF was detected within a single parasite cycle. Ring and nonpigmented trophozoite stages were sensitive to the inhibitory effect of DF but cytostatic antimalarial activity was suggested by evidence of parasite recovery in later cycles. However, profound growth inhibition, with no evidence of subsequent recovery, occurred when pigmented trophozoites and early schizonts were exposed to DF. At this stage in parasite development, the activity of DF was cytocidal and furthermore, the critical period of exposure may be as short as 6 hours. These observations suggest that iron chelators may have a role in the treatment of clinical malaria.

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