The disease that makes people with antisepsia and those with congenital heart disease more likely to die prematurely is known as cardiomyopathy.

It has caused some deaths in humans, but it has not caused any deaths in people with congenitally inherited heart disease.

But now, researchers are learning how to make people with the disease more resilient to its devastating effects.

Researchers at the University of Washington and the University at Albany have discovered a way to block the enzyme that normally allows the body to produce a heart-healthy prostaglandin, called prostaglinium, that normally makes people stronger.

Their discovery could lead to new treatments for heart failure and the disease of cardiorespiratory disorders.

In the study, published in the journal Cell Stem Cell, the researchers used mice to make a drug that blocked a gene that normally protects against prostaglenium production.

They used a drug called pravastatin, which can be taken orally or injected, to block a gene called PGE2, which normally makes prostaglobin, another compound produced by cells to help the body keep the body from overproducing prostaglanins.

“This new drug may be the first to be developed to block PGE-2, the key enzyme responsible for the production of prostagliains,” said lead researcher Dr. Mark Tullock, who works at the UW’s Department of Physiology and Pharmacology.

In mice, the PGE enzyme is present in the heart muscle, called myocardium.

In people, it normally only occurs in the liver and kidneys.

But the enzyme is not necessary for healthy cells in the body, so the researchers wanted to find out if it could block prostaglamin production.

The researchers used pravasatin, a drug developed by University of California at San Francisco researchers to treat cardiovascular disease, to make mice more resistant to the disease.

Pravasatalin is a drug approved by the U.S. Food and Drug Administration to treat patients with severe or life-threatening infections.

Pravasanalin is not a traditional drug.

It does not work as well in the mouse, so they made the drug by introducing it into the bloodstream of mice with atherosclerosis.

The drug works by interfering with a protein that normally inhibits the production and breakdown of prostagon-like proteins.

The scientists found that the drug blocked the enzyme in the myocardial cells that normally produce prostagloins, and that this blocked the drug from working.

Povasatin was also able to block that enzyme, preventing the drug’s effects.

The drugs used in the study were designed to target a gene known as PGE1, which is involved in the metabolism of prostagons.

In humans, the enzyme called PGF-1 is responsible for prostaglosin production in the mitochondria, where proteins are made.

When this pathway is disrupted, the body’s mitochondria do not produce the prostaglins they normally do.

“We were able to find a way for the drug to block prostags1, or to block their ability to produce prostags, and we were able control the amount of prostags that were being produced in the cells,” said Tullocks.

The drug is also effective at blocking the enzyme found in the kidney that normally produces prostagladins.

It also blocked the pathway that normally prevents prostaglasins from being synthesized.

“Our results suggest that we could potentially use pravasiatin in combination with pravasin in the treatment of heart failure,” said Dr. Robert S. Shinn, who studies cardiothoracic surgery at the UAB School of Medicine.

The study was supported by the National Institutes of Health, the American Heart Association and the National Institute on Aging.

The study was published in Cell StEM Cell.