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Doctors have a new way to treat ‘soreness’

A doctor has invented a treatment that could reduce symptoms of common colds by turning off the body’s natural immune response.

Dr. Shoshana M. Houshmandar and her colleagues at Mount Sinai School of Medicine in New York have created a drug that turns off the immune system in mice.

The new treatment works by blocking a protein called Toll-like receptor-4 (TLR4), which is normally activated by colds.

The treatment is so effective that Houshat’s team is now trying to apply it to humans.

“We’re not using it as a vaccine, but we’re trying to turn off the inflammatory response,” Houshamandar said in a statement.

“We think it’s a way to be proactive and help patients stay healthy while they’re getting the treatments they need.”

In a new study published in the journal Nature Medicine, Houshas found that mice treated with the drug had better immune response to the common cold than mice treated alone.

“I think the results are very exciting because there are some other therapies that have shown to be successful in this field,” said senior author Dr. Jeffrey M. Kiely, a microbiologist at Mount Columbia University School of Public Health in New Jersey.

Kiely said that while the study was limited by the small sample size, the drug could be a significant step forward in the fight against the common disease.

The common cold causes a variety of symptoms that can cause long-term health problems, including coughing, runny nose and runny eyes.

Many people with the cold have difficulty getting a cold vaccine, because it’s made by different companies and is different in formula.

In order to create the vaccine, Hosehat’s group needed to develop an immune-modulating molecule that would target TLR4.

To do that, the team looked at the natural antibodies produced by immune cells, called monocytes.

Houshhadar’s team tested the compounds that the monocytes produced against the antibody.

They found that the molecules that they used to produce antibodies could knock down TLR1, the molecule that’s responsible for activating immune cells.

Kieshmandars team also found that monocytes treated with an anti-TLR1 antibody did not produce more cytokines, which are the body response to infection and stress.

Kierly said the study’s findings suggest that TLR2 may be a key component in the immune response that can trigger inflammation.

TLR3, the enzyme that produces cytokines and is activated by infections and stress, may also be important in triggering inflammation, KieshMandar said.

To make the vaccine in mice, the scientists turned off TLR6 in the body and turned it back on again.”TLR6 and TLR5 are involved in the inflammatory responses,” Kieshed said.

“So, if we can turn on TLR7, we can knock down the inflammation and decrease inflammation in mice.”

The researchers said the drug was already in the pipeline, and the researchers had the approval to start human trials in about a year.