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Month: October 2012 (page 2 of 10)

10.25.2012

new treatments for food allergies

Food allergies are caused when an IgE antibody is produced in response to a protein from the food in question. This has lead scientists to believe that IgE could be a potential drug target for allergy treatments. From C&EN:

One treatment aimed at IgE that’s already commercially available is omalizumab. Comarketed by Genentech and Novartis under the brand name Xolair, this therapeutic is a monoclonal antibody designed to mop up free IgE in a person’s body.

“An ordinary antibody to IgE could kill people,” says Tse Wen Chang, originator of the anti-IgE concept and a distinguished research fellow at Academia Sinica, in Taiwan. That’s because if the antibody stuck to IgEs that were already bound to mast cells and basophils, the interaction might trigger anaphylaxis via histamine and those other inflammatory compounds.

“So you can imagine that when I approached people initially with the idea, they were very concerned,” Chang says. This was in 1989, soon after Chang had cofounded a small biopharmaceutical firm called Tanox. He was looking for a corporate partner to fund the company’s anti-IgE program.

Chang eventually convinced Tanox’ potential partners and others in the immunology field that his IgE antibodies were safe. He demonstrated that the therapeutics, screened and selected during synthesis, bind free IgE and not mast-cell-bound IgE. After a partnership with Novartis, a few infamous legal disputes with Genentech, some clinical trials, and an eventual buyout by Genentech in 2007, Tanox disappeared from the pharma scene.

But the anti-IgE concept, in the form of Xolair, has lived on. The monoclonal antibody was approved in 2003 by the Food & Drug Administration for use in patients with moderate to severe persistent cases of asthma. The injectable therapeutic is now involved in more than 100 clinical trials for various types of allergies, including for the treatment of chronic hives and eczema.

Xolair hasn’t made as much headway, though, in treating food allergies, Chang says. A small study, published last year, aimed to test whether peanut-allergy sufferers could benefit from regular injections of the antibody (J. Allergy Clin. Immunol., DOI: 10.1016/j.jaci.2011.01.051). But the trial was discontinued because a few patients had severe anaphylactic reactions to test-doses of peanuts—given to them prior to Xolair—and a safety committee deemed the experiment too risky.

….

So food allergists haven’t given up on Xolair. Instead of being used by itself, the antibody is now being administered in combination with oral immunotherapy: Phase I and Phase II trials are under way to see whether the therapeutic can improve the outcome of milk- and peanut-allergy treatments.

10.24.2012

fighting disease through cloning

Swapping one woman’s nuclear DNA for another can reduce the incidence of inherited diseases caused by mitochondrial misregulation. From Science News:

A technique that puts one woman’s nuclear DNA into another woman’s donor egg cell may be feasible for correcting inherited diseases caused by faulty cellular power sources. The technique has already produced healthy baby rhesus monkeys, and now it raises the possibility of preventing mitochondrial diseases in thousands of people each year.

Mitochondria, energy-producing organelles inside cells, carry circles of DNA important for the power plants’ function. Mutations of the mitochondrial DNA, which is passed to offspring directly by their mothers, can cause diseases that often affect energy-greedy organs such as the brain, heart, muscles, pancreas and kidneys with varying severity. An estimated 1,000 to 4,000 U.S. babies are born each year with mitochondrial diseases.

Swapping the nucleus, the cellular compartment where chromosomes are housed, from an egg with mutant mitochondria into one containing functional power plants could stop those diseases from happening in the first place. Offspring would inherit healthy mitochondria from the egg donor, while the rest of their genetic makeup would come from the mother and father.

Researchers led by Shoukhrat Mitalipov, a reproductive and developmental biologist at Oregon Health & Science University in Beaverton, previously demonstrated that the technique works with rhesus monkeys. Now the team has succeeded in transferring the nuclei of unfertilized human eggs into donor eggs and then fertilizing those eggs to create embryos that produce embryonic stem cells, the team reports online October 24 in Nature. Short of actually transplanting the embryos into women to grow into babies, stem cell production is the clearest sign that the embryos are normal.

Performing the transfer procedure in the United States for women who carry faulty mitochondria, and implanting resulting embryos in the womb, will require approval of the federal Food and Drug Administration, which oversees clinical trials involving gene therapy.

Although the experimental therapy requires transfer of a nucleus into an egg, as human cloning would, it does not raise the same ethical concerns as human cloning, says Josephine Johnston, a research scholar at the Hastings Center, an organization in Garrison, N.Y., that examines the ethics of biological research. “To me it’s not human cloning,” Johnston says. “It’s not the creation of an individual who is genetically identical to an existing person.”

10.23.2012

on the origins of blood types

Different antigens are present in A,B, AB and O type blood.

Humans can have blood types A, B, AB or O depending on what type of antigens are present on their red blood cells. A recent study in PNAS determined that these blood types existed in early humans and even in apes and chimps. From Science News:

Different forms of a single blood type gene determine what types of molecules sit on your red blood cells: type A molecules, type B molecules, A and B together, or no intact surface molecules in the case of type O (O was originally called type C, then was changed to O for the German “ohne,” meaning “without”).

The A, B and O versions of the gene differ only slightly, and scientists have debated two scenarios to explain their evolution. One posits that the A version of the gene existed long ago, and the B and/or O versions later cropped up independently in several species (including humans, gorillas, baboons and chimps). Alternatively, all of those species may have inherited the A and B types from a single ancestor.

To get some bloody perspective on the matter, researchers led by Ségurel looked at a particular stretch of DNA in the blood type gene in humans, bonobos, chimpanzees, gorillas, orangutans and several species of monkey. Then the scientists compared that stretch of DNA across species on the larger primate family tree. The pattern they saw suggests that the A and B blood groups were around at least 20 million years ago, well before the chimp-human split, and probably as far back as the common ancestor of humans and old-world monkeys. Sections of DNA in the human A version, for example, more closely matched the A version that gibbons have than the human B version of the gene.

Exactly why evolution would favor a mix of blood types in so many species is a mystery. Depending on blood type, people are more or less susceptible to particular pathogens. Type O people, for example, are more susceptible to cholera and plague, while people with type A are more susceptible to smallpox. Blood group diversity may have been maintained for so long because each version was immunologically advantageous in certain times and places.

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