Sentences with phrase «cell by the malaria»

Scientists from Singapore's Nanyang Technological University (NTU) have discovered a key process during the invasion of the blood cell by the Malaria parasite, and more importantly, found a way to block this invasion.

The newly invented technique utilises a high - throughput fluorescence scanning approach — if antibodies or drugs fail to prevent the invasion of the red blood cell by the malaria parasites, the sample will light up.

Not exact matches

By contrast, women who carry a sickle - cell allele, which protects against malaria, have only about 50 percent more surviving children in malaria - infested regions than women lacking the variant.

Researchers at Harvard T. H. Chan School of Public Health and the Broad Institute have identified a protein on the surface of human red blood cells that serves as an essential entry point for invasion by the malaria parasite.

Scientists have identified a protein on the surface of human red blood cells that serves as an essential entry point for invasion by the malaria parasite.

The risk of developing severe malaria turns out to be strongly linked to the process by which the malaria parasite gains entry to the human red blood cell.

First, after a person is bitten by a parasite - carrying mosquito there is an initial infection in the liver, followed by the long - lasting red blood cell stage where the clinical symptoms of the malaria disease occur, and finally the mosquito stage, which is required to transmit the parasites to other people.

But now University of Pennsylvania biochemist Doron Greenbaum has found a way to lock malaria inside the cells by blocking the action of a key host protein, called calpain, that allows its escape.

The gene codes for an immune receptor on red blood cells; lack of that receptor prevents infection by Plasmodium vivax, a species of the malaria parasite.

Apparently, antibodies to this protein protected against malaria by trapping the schizont inside the red blood cell — not by preventing it from infecting new ones.

Snell is particularly encouraged by the possibility of controlling malaria, which is caused by the single - celled protozoan Plasmodium falciparum.

Microbes that cause diseases like HIV, malaria, and hepatitis C exploit and often activate the same checkpoint pathways — cell surface receptors such as CTLA4 and PD - 1 — to slow immune cells and prevent their elimination by the host.

«Our study shows that the ability of malaria parasites to engage red blood cells is driven by an ancient mechanism for cellular attachment,» said lead author Aditya Paul, a postdoctoral researcher at the Harvard Chan School.

Malaria is caused by a single - celled parasite called Plasmodium that spreads from person to person through mosquito bites.

In 2008, researchers led by YongKeun Park and Monica Diez - Silva of the Massachusetts Institute of Technology found that red blood cells vibrated less when they were infected with the malaria parasite, apparently because the infection made the cells stiffer than normal (Proceedings of the National Academy of Sciences, DOI: 10.1073 / pnas.0806100105).

A new study shows that a 70 - year - old malaria drug can block immune cells in the liver so nanoparticles can arrive at their intended tumor site, overcoming a significant hurdle of targeted drug delivery, according to a team of researchers led by Houston Methodist.

It built on previous ground - breaking work on malaria published in 2011 by author Monash Professor Christian Doerig, and others, who found that if host cell protein kinases were prevented from working it would kill malaria parasites.

Malaria is a life - threatening disease caused by a parasite that invades one red blood cell after another.

«Many researchers are trying to find ways to develop a malaria vaccine by preventing the parasite from entering the red blood cell, and here we found a way to block it from leaving the cell once it has entered.

Avian malaria is mainly caused by the parasite Plasmodium relictum, which reproduces in red blood cells.

Dr. Jonathan Kurtis, professor of pathology and laboratory medicine at Brown, made global headlines last year when he and colleagues revealed a promising protein that combats malaria by preventing the parasite from exiting red blood cells to spread.

The malaria parasite survives in its host by remodeling the red blood cells in which it dwells.

Malaria results from infection of human red blood cells (RBC) by the plasmodium parasite.

By teasing apart the structure of an enzyme vital to the parasites that cause toxoplasmosis and malaria, Whitehead Institute scientists have identified a potentially «drugable» target that could prevent parasites from entering and exiting host cells.

Her newest project, funded by the National Institute of Allergy and Infectious Diseases of the National Institutes of Health, will look at the crucial time when malaria is transmitted — when reproductive cell precursors known as gametocytes develop.

Peter Agre, MD, professor and director of the Johns Hopkins Malaria Research Institute, was among the scientists and policymakers attending the March 9 signing of the Stem Cell Executive Order and Presidential Memorandum on Scientific Integrity by President Barack Obama.

Malaria is caused by species of single - celled parasites in the genus Plasmodium, vectored by mosquitoes primarily in the genera Aedes and Anopheles between many vertebrate hosts, including humans.

«Most vaccine candidates for malaria have worked by trying to prevent parasites from entering red blood cells,» said Dr Jonathan Kurtis of Rhode Island Hospital, the team's spokesman.