Hungry Insects, Skull Channels, and a New Drug for Treating Malaria

Scientific Research News Clip 2

Warmer Temperatures Increase the Appetite of Insects

A new study in Science (August 31) estimates that each degree Celsius rise of warming temperature will result in an extra 10 to 25 percent of crop losses.


This prediction was made by Curtis Deutsch and his colleagues of the University of Washington in Seattle, based on how heat may speed up insects' metabolism and reproduction.

Yearly, the damage by insects are 8% to maize and wheat, 14% to rice. If the temperature rises 2 degrees Celsius, annual losses would be 10%, 12% and 17% for maize, wheat and rice, respectively. In other words, about 213 million tons of the three grains combined will be lost totally.

According to Deutsch, the whole Europe, east and central U.S., coastal areas of China would see the biggest damage to maize by the end of the century because of its milder climates; while the damage in tropical areas is less as those places are already near the insects' tolerance for high temperatures and with the lower insect reproduction.

Nathan Lemoine, physiological ecologist of Colorado State University in Fort Collins, praised the study "an incredibly valuable first step" to predicting future crop losses caused by warming temperatures. But he notes that insect metabolism could only be one of the many factors related to the crop yields in the future.

As the Earth warms, insects become hungrier, which means bigger losses of crops. Although the damage is not a sky-is-falling, people would better face such a threat and adopt some new defenses against the crop-munching insects.

Skull Channels Speed Up Immune Cells to Reach the Brain

Some scientists had thought that neutrophils (immune cells) traveled to the brain by coming equally from all sources of bone marrow, such as arm, leg, pelvis and skull.


However, Matthias Nahrendorf of Massachusetts General Hospital and Harvard Medical School and his colleagues reported August 27 in
Nature Neuroscience that inflammatory immune cells come to the brain mostly from skull marrow cutting through the tiny skull channels.

Scientists found this new path by injecting dyes into skull and other bone marrow of the mice. These channels are 22 micrometers across on average and connect skull marrow to the outer brain membrane in mice.

It's not known yet whether immune cells use these skull channels in people—77 micrometers across on average—as it does in mice, though skull bones are riddled with microscopic channels.

Many brain diseases including acute stroke, hypertension and Alzheimer, etc., have inflammatory substances, so scientists will next investigate the relevance of skull channels to those brain diseases, and the function of these channels. Besides, skull channels could serve as a path to deliver drugs from skull marrow to the meninges, as Nahrendorf said.

A New Drug Called Tafenoquine Is Approved by FDA to Eradicate Malaria

 Anopheles albimanus mosquito
Plasmodium vivax is a stubborn kind of malaria because of its relapse in infected people. It is spread by the Anopheles mosquito, causing chills, a cyclical fever and joint aches, and can stay in the liver of a body for weeks or months.

Once the people infected with P. vivax are bitten by a mosquito, the parasite then returns to the bloodstream and cause the relapse of malaria.

Tafenoquine (or with the name Krintafel in the U.S. market) is just targeting such a relapsing malaria. It was approved by FDA in July as a new treatment for this recurring disease. And though the treatment can cause a dangerous side effect, tafenoquine might be the right drug to eradicate malaria.

About 8.5 million people are infected with P. vivax, mainly in Asia and Latin America. And the countries in these areas are more likely expected to follow FDA by approving tafenoquine for malaria treatment.

Compared with primaquine, another older drug treating malaria relapses, tafenoquine is more effective in the treatment with its compressed dosing schedule and no drug resistance.

However, both primaquine and tafenoquine can cause a dangerous side effect in people with G6PD (glucose-6-phosphate dehydrogenase) deficiency. About 400 million people in the world are affected by G6PD deficiency—a variation on the X chromosome. When these people take either of the two drugs, they get high risk of destroying their red blood cells, i.e., hemolytic anemia.

Because tafenoquine can stay in the body for long and is hard to be cleared out by the body itself, people with G6PD deficiency are certainly unavoidable at a higher risk for hemolytic anemia.

The test for the identification of genetic deficiency is essential when the drug is put to use in places like rural areas with high rates of both P. vivax and such a deficiency. Since the test is complicated as well as its lab facilities, it's not achievable for the developing countries where relapsing malaria is endemic, for example, in Asia and South America, to do the deficiency test.

A new version of the test is under development backed up by PATH, a nonprofit global health organization in Seattle. In the test, people only need a finger prick and are advised to take a relatively safe treatment— a low-dose of primaquine for two months— if they test positive for G6PD deficiency.

The new G6PD deficiency test which has its field trials in Ethiopia, Brazil and India is "a great tool for people to use tafenoquine safely," said Gonzalo Domingo, a scientific director at PATH.

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