scholarly journals A high parasite density environment induces transcriptional changes and cell death in Plasmodium falciparum blood stages

FEBS Journal ◽  
2018 ◽  
Vol 285 (5) ◽  
pp. 848-870 ◽  
Author(s):  
Evelyn S. Chou ◽  
Sabia Z. Abidi ◽  
Marian Teye ◽  
Aleksandra Leliwa‐Sytek ◽  
Thomas S. Rask ◽  
...  
Keyword(s):  
Cell Death ◽  
Plasmodium Falciparum ◽  
Parasite Density ◽  
High Parasite Density ◽  
Transcriptional Changes ◽  
High Parasite

scholarly journals HUBUNGAN STATUS GIZI DENGAN TINGKAT KEPADATAN PARASIT MALARIA PADA ANAK

e-CliniC ◽  
2016 ◽  
Vol 4 (1) ◽  
Author(s):  
Jeanette Elmerose Natalia Lee ◽  
Suryadi N. N. Tatura ◽  
Hesti Lestari
Keyword(s):  
Nutritional Status ◽  
Parasite Density ◽  
Malaria Parasite ◽  
Inclusion Criteria ◽  
Significant Relation ◽  
Cross Sectional ◽  
Gamma Correlation ◽  
High Parasite Density ◽  
Cross Sectional Design ◽  
High Parasite

Latar belakang: Status gizi diketahui dapat mempengaruhi kepadatan parasit malaria pada anak, sehingga melalui status gizi dapat dinilai tingkat kepadatan parasit malaria. Namun status gizi bukan merupakan satu-satunya faktor yang menyebabkan tingginya kepadatan parasit malaria, terdapat faktor lain yang turut berperan dalam hal ini. Tujuan: Untuk mengetahui hubungan antara status gizi dengan tingkat kepadatan parasit malaria. Metode: Penelitian ini menggunakan metode penelitian analititik retrospektif dengan pendekatan potong lintang (cross sectional). Sampel penelitian sebanyak 59 anak yang memenuhi kriteria inklusi. Data dianalisis menggunakan uji koefisien korelasi Gamma. Hasil: Dari 65 anak didapatkan 59 sebagai sampel penelitian yang memnuhi kriteria inklusi. Status gizi dengan kepadatan parasit malaria didapatkan kepadatan tinggi dengan gizi kurang sebanyak 9 anak (15,3%), dengan gizi baik sebanyak 24 anak (40,7%), dengan overweight sebanyak 2 anak (3,4%) dan dengan obesitas sebanyak 2 anak (3,4%). Sedangkan kepadatan rendah dengan gizi kurang sebanyak 9 anak (8,5%), dengan gizi baik sebanyak 13 anak (22,0%), dengan overweight sebanyak 3 anak (5,1%). Dengan uji koefisien korelasi Gamma didapatkan korelasi yang sangat lemah (rG = 0,118; p = 0,632). Hasil ini menyatakan bahwa tidak terdapat hubungan yang bermakna antara status gizi dengan kepadatan parasit malaria.Kesimpulan: Tidak terdapat hubungan yang bermakna antara status gizi dengan tingkat kepadatan parasit malaria pada anak.Kata kunci: Malaria, kepadatan parasit, status gizi, anak.Background: Nutritional status can influence malaria parasite density in children, so from nutritional status we can evaluate malaria parasite density. Nutritional status is not the only factor which cause high malaria parasite density, there are another factors which cause this. Objective: To find out the relation between nutritional status and malaria parasite density in children. Methods: This study uses analytic retrospective method with cross –sectional design. About 59 sample qualify the inclusion criteria. Data were analyzed using Gamma correlation coefficient statistical test. Results: From 65 children, there are 59 children who qualify the inclusion criteria. On the analysis of nutritional status and malaria parasite density, children with high parasite density consist of 9 children (15,3%) with malnutrition, 24 children (40,7%) with good nutritional status, 2 children (3,4%) with overweight, and 2 children (3,4%) with obesity. On children with low parasite density, there are 9 children (8,5%) with malnutrition, 13 children (22,0%) with good nutritional status, and 3 children (5,1%) with overweight. Using Gamma correlation test, the study find a very weak correlation (rG = 0,118; p = 0,632). This find indicates that there is no significant relation between nutritional status and malaria parasite density. Conclusion: There is no significant relation between nutritional status and malaria parasite density in children.Keywords: Malaria, parasite density, nutritional status, children.

scholarly journals Seasonality and Malaria in a West African Village: Does High Parasite Density Predict Fever Incidence?

1997 ◽  
Vol 145 (9) ◽  
pp. 850-857 ◽  
Author(s):  
P. Bouvier ◽  
A. Rougemont ◽  
N. Breslow ◽  
O. Doumbo ◽  
V r. Delley ◽  
...  
Keyword(s):  
Parasite Density ◽  
West African ◽  
High Parasite Density ◽  
High Parasite

Life cycle of Babesia argentina (Lignières, 1903) (Sporozoa : Piroplasmidea) in the tick vector Boophilus microplus (Canestrini)

1966 ◽  
Vol 17 (2) ◽  
pp. 247 ◽  
Author(s):  
RF Riek
Keyword(s):  
Parasite Density ◽  
Subsequent Development ◽  
Protozoan Parasite ◽  
Adult Tick ◽  
Boophilus Microplus ◽  
Babesia Bigemina ◽  
Larval Attachment ◽  
Multiple Fission ◽  
High Parasite Density ◽  
High Parasite

Babesia argeutina, a protozoan parasite causing tick fever of cattle in Australia, is transmitted by Boophilus microplus. Its development in this invertebrate vector is very similar to that recorded by Riek (1964) for Babesia bigemina. Many of the parasites occurring in the bovine erythrocytes are destroyed on ingestion but the early development in the lumen of the gut is uncertain. By about 36 hr, blunt, cigar-shaped forms, 7.2–1 3.8 µ by 2.6–5.6 µ, invade the epithelial cells of the gut and subsequent development is by means of multiple fission. This leads, by about 96 hr, to the production of mature vermicules which measure about 15.8 µ by 3.0 µ, with a range of 14.3–16.9 µ by 2.8–3.5 µ. At about this time vermicules enter the mature ova of the tick, and a further cycle of multiple fission in the gut cells of the developing larva gives rise to vermicules similar to those produced in the adult tick. The final cycle takes place in the salivary glands of the larva, and the forms infective to the vertebrate host appear 2–3 days and longer after larval attachment. Multiplication in this cycle is also by multiple fission and gives rise to comparatively small numbers of infective forms measuring about 1.5 µ by 1.0 µ. Not all ticks develop an infection even after engorging on blood with a high parasite density. Certain 'strains' of Boophilus microplus seem to be more susceptible to infection than others. Heavy mortalities occurred in many ticks after ingesting blood with a parasite density of 5% or higher.

Toxoplasma Gondii Bradyzoites Elicit Transcriptional Changes in Host Cells to Prevent IFNγ-Mediated Cell Death

2019 ◽  
Author(s):  
Simona Seizova ◽  
Alexandra L Garnham ◽  
Michael J Coffey ◽  
Lachlan W Whitehead ◽  
Kelly L Rogers ◽  
...  
Keyword(s):  
Cell Death ◽  
Toxoplasma Gondii ◽  
Host Cells ◽  
Transcriptional Changes

scholarly journals Ferroptotic cell death triggered by conjugated linolenic acids is mediated by ACSL1

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Alexander Beatty ◽  
Tanu Singh ◽  
Yulia Y. Tyurina ◽  
Vladimir A. Tyurin ◽  
Svetlana Samovich ◽  
...  
Keyword(s):  
Cell Death ◽  
Therapeutic Potential ◽  
Neutral Lipids ◽  
Cell Types ◽  
Lipid Hydroperoxides ◽  
Conjugated Linolenic Acids ◽  
Cellular Lipids ◽  
Transcriptional Changes ◽  
Acyl Chains ◽  
Tumor Growth And Metastasis

AbstractFerroptosis is associated with lipid hydroperoxides generated by the oxidation of polyunsaturated acyl chains. Lipid hydroperoxides are reduced by glutathione peroxidase 4 (GPX4) and GPX4 inhibitors induce ferroptosis. However, the therapeutic potential of triggering ferroptosis in cancer cells with polyunsaturated fatty acids is unknown. Here, we identify conjugated linoleates including α-eleostearic acid (αESA) as ferroptosis inducers. αESA does not alter GPX4 activity but is incorporated into cellular lipids and promotes lipid peroxidation and cell death in diverse cancer cell types. αESA-triggered death is mediated by acyl-CoA synthetase long-chain isoform 1, which promotes αESA incorporation into neutral lipids including triacylglycerols. Interfering with triacylglycerol biosynthesis suppresses ferroptosis triggered by αESA but not by GPX4 inhibition. Oral administration of tung oil, naturally rich in αESA, to mice limits tumor growth and metastasis with transcriptional changes consistent with ferroptosis. Overall, these findings illuminate a potential approach to ferroptosis, complementary to GPX4 inhibition.

scholarly journals IMiDs prime myeloma cells for daratumumab-mediated cytotoxicity through loss of Ikaros and Aiolos

Blood ◽  
2018 ◽  
Vol 132 (20) ◽  
pp. 2166-2178 ◽  
Author(s):  
Pasquale L. Fedele ◽  
Simon N. Willis ◽  
Yang Liao ◽  
Michael S. Low ◽  
Jai Rautela ◽  
...  
Keyword(s):  
Cell Death ◽  
Regulatory Networks ◽  
Nk Cell ◽  
Surface Expression ◽  
Nucleosome Remodeling ◽  
Interferon Stimulated Genes ◽  
Cd38 Expression ◽  
Cycle Arrest ◽  
Transcriptional Changes ◽  
Insight Into

Abstract Recent studies have demonstrated that the immunomodulatory drugs (IMiDs) lead to the degradation of the transcription factors Ikaros and Aiolos. However, why their loss subsequently leads to multiple myeloma (MM) cell death remains unclear. Using CRISPR-Cas9 genome editing, we have deleted IKZF1/Ikaros and IKZF3/Aiolos in human MM cell lines to gain further insight into their downstream gene regulatory networks. Inactivation of either factor alone recapitulates the cell intrinsic action of the IMiDs, resulting in cell cycle arrest and induction of apoptosis. Furthermore, evaluation of the transcriptional changes resulting from their loss demonstrates striking overlap with lenalidomide treatment. This was not dependent on reduction of the IRF4-MYC “axis,” as neither protein was consistently downregulated, despite cell death occurring, and overexpression of either factor failed to rescue for Ikaros loss. Importantly, Ikaros and Aiolos repress the expression of interferon-stimulated genes (ISGs), including CD38, and their loss led to the activation of an interferon-like response, contributing to MM cell death. Ikaros/Aiolos repressed CD38 expression through interaction with the nucleosome remodeling and deacetylase complex in MM. IMiD-induced loss of Ikaros or treatment with interferon resulted in an upregulation of CD38 surface expression on MM cells, priming for daratumumab-induced NK cell-mediated antibody-dependent cellular cytotoxicity. These results give further insight into the mechanism of action of the IMiDs and provide mechanistic rationale for combination with anti-CD38 monoclonal antibodies.

scholarly journals Analysis of the clinical profile in patients with Plasmodium falciparum malaria and its association with parasite density

2017 ◽  
Vol 9 (2) ◽  
pp. 60 ◽  
Author(s):  
Praveen Mangal ◽  
Shilpa Mittal ◽  
Kamal Kachhawa ◽  
Divya Agrawal ◽  
Bhabagrahi Rath ◽  
...  
Keyword(s):  
Plasmodium Falciparum ◽  
Falciparum Malaria ◽  
Parasite Density ◽  
Plasmodium Falciparum Malaria ◽  
Clinical Profile
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