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Mommy2Alysa

New member
WOOHOO This was happening right at my work place! So exciting... it was in the paper this morning and I had to share

Breakthrough holds promise for cystic fibrosis

By Communications Staff
Wednesday, July 30, 2008

A University of Western Ontario professor studying cystic fibrosis (CF) has successfully corrected the defect which causes the overproduction of intestinal mucous in mice.



This discovery by Richard Rozmahel, an associate professor of Biochemistry, Pediatrics and Oncology at the Schulich School of Medicine & Dentistry and scientist with the Lawson Health Research Institute, has clear implications to understanding and treating this facet of the disease in humans.


Cystic fibrosis is a fatal, genetic disease affecting 70,000 children and adults worldwide, and characterized by an overproduction of mucous in the lungs and digestive system. Compared to the 1960's, when most patients died by age four, the median age of survival is now 37 years.

Rozmahel and his colleagues are identifying secondary genes that could contribute to CF, and measuring their impact on the disease. More specifically, they are investigating the potential of a gene found in mice, mCLCA3, which is similar to one in humans that exhibits abnormal levels in CF. The mCLCA3 gene is expressed by cells that produce and secrete mucous.

The researchers discovered that mCLCA3 plays an important role in the property of mucous, thereby allowing it to be cleared rather than result in the blockages that underlie CF. By correcting the abnormal levels of mCLCA3 in CF mice they were able to overcome the mucous lesions.

Whereas CF mice normally do not survive more than four weeks as a consequence of the mucous disease, the animals where mCLCA3 levels were corrected could live a normal lifespan.

"It's my hope to understand what is causing the exaggerated mucous production and secretion in CF patients," says Dr. Rozmahel. "From there, we can figure out ways to correct it."
 

Mommy2Alysa

New member
WOOHOO This was happening right at my work place! So exciting... it was in the paper this morning and I had to share

Breakthrough holds promise for cystic fibrosis

By Communications Staff
Wednesday, July 30, 2008

A University of Western Ontario professor studying cystic fibrosis (CF) has successfully corrected the defect which causes the overproduction of intestinal mucous in mice.



This discovery by Richard Rozmahel, an associate professor of Biochemistry, Pediatrics and Oncology at the Schulich School of Medicine & Dentistry and scientist with the Lawson Health Research Institute, has clear implications to understanding and treating this facet of the disease in humans.


Cystic fibrosis is a fatal, genetic disease affecting 70,000 children and adults worldwide, and characterized by an overproduction of mucous in the lungs and digestive system. Compared to the 1960's, when most patients died by age four, the median age of survival is now 37 years.

Rozmahel and his colleagues are identifying secondary genes that could contribute to CF, and measuring their impact on the disease. More specifically, they are investigating the potential of a gene found in mice, mCLCA3, which is similar to one in humans that exhibits abnormal levels in CF. The mCLCA3 gene is expressed by cells that produce and secrete mucous.

The researchers discovered that mCLCA3 plays an important role in the property of mucous, thereby allowing it to be cleared rather than result in the blockages that underlie CF. By correcting the abnormal levels of mCLCA3 in CF mice they were able to overcome the mucous lesions.

Whereas CF mice normally do not survive more than four weeks as a consequence of the mucous disease, the animals where mCLCA3 levels were corrected could live a normal lifespan.

"It's my hope to understand what is causing the exaggerated mucous production and secretion in CF patients," says Dr. Rozmahel. "From there, we can figure out ways to correct it."
 

Mommy2Alysa

New member
WOOHOO This was happening right at my work place! So exciting... it was in the paper this morning and I had to share

Breakthrough holds promise for cystic fibrosis

By Communications Staff
Wednesday, July 30, 2008

A University of Western Ontario professor studying cystic fibrosis (CF) has successfully corrected the defect which causes the overproduction of intestinal mucous in mice.



This discovery by Richard Rozmahel, an associate professor of Biochemistry, Pediatrics and Oncology at the Schulich School of Medicine & Dentistry and scientist with the Lawson Health Research Institute, has clear implications to understanding and treating this facet of the disease in humans.


Cystic fibrosis is a fatal, genetic disease affecting 70,000 children and adults worldwide, and characterized by an overproduction of mucous in the lungs and digestive system. Compared to the 1960's, when most patients died by age four, the median age of survival is now 37 years.

Rozmahel and his colleagues are identifying secondary genes that could contribute to CF, and measuring their impact on the disease. More specifically, they are investigating the potential of a gene found in mice, mCLCA3, which is similar to one in humans that exhibits abnormal levels in CF. The mCLCA3 gene is expressed by cells that produce and secrete mucous.

The researchers discovered that mCLCA3 plays an important role in the property of mucous, thereby allowing it to be cleared rather than result in the blockages that underlie CF. By correcting the abnormal levels of mCLCA3 in CF mice they were able to overcome the mucous lesions.

Whereas CF mice normally do not survive more than four weeks as a consequence of the mucous disease, the animals where mCLCA3 levels were corrected could live a normal lifespan.

"It's my hope to understand what is causing the exaggerated mucous production and secretion in CF patients," says Dr. Rozmahel. "From there, we can figure out ways to correct it."
 

Mommy2Alysa

New member
WOOHOO This was happening right at my work place! So exciting... it was in the paper this morning and I had to share

Breakthrough holds promise for cystic fibrosis

By Communications Staff
Wednesday, July 30, 2008

A University of Western Ontario professor studying cystic fibrosis (CF) has successfully corrected the defect which causes the overproduction of intestinal mucous in mice.



This discovery by Richard Rozmahel, an associate professor of Biochemistry, Pediatrics and Oncology at the Schulich School of Medicine & Dentistry and scientist with the Lawson Health Research Institute, has clear implications to understanding and treating this facet of the disease in humans.


Cystic fibrosis is a fatal, genetic disease affecting 70,000 children and adults worldwide, and characterized by an overproduction of mucous in the lungs and digestive system. Compared to the 1960's, when most patients died by age four, the median age of survival is now 37 years.

Rozmahel and his colleagues are identifying secondary genes that could contribute to CF, and measuring their impact on the disease. More specifically, they are investigating the potential of a gene found in mice, mCLCA3, which is similar to one in humans that exhibits abnormal levels in CF. The mCLCA3 gene is expressed by cells that produce and secrete mucous.

The researchers discovered that mCLCA3 plays an important role in the property of mucous, thereby allowing it to be cleared rather than result in the blockages that underlie CF. By correcting the abnormal levels of mCLCA3 in CF mice they were able to overcome the mucous lesions.

Whereas CF mice normally do not survive more than four weeks as a consequence of the mucous disease, the animals where mCLCA3 levels were corrected could live a normal lifespan.

"It's my hope to understand what is causing the exaggerated mucous production and secretion in CF patients," says Dr. Rozmahel. "From there, we can figure out ways to correct it."
 

Mommy2Alysa

New member
WOOHOO This was happening right at my work place! So exciting... it was in the paper this morning and I had to share
<br />
<br />Breakthrough holds promise for cystic fibrosis
<br />
<br />By Communications Staff
<br />Wednesday, July 30, 2008
<br />
<br />A University of Western Ontario professor studying cystic fibrosis (CF) has successfully corrected the defect which causes the overproduction of intestinal mucous in mice.
<br />
<br />
<br />
<br />This discovery by Richard Rozmahel, an associate professor of Biochemistry, Pediatrics and Oncology at the Schulich School of Medicine & Dentistry and scientist with the Lawson Health Research Institute, has clear implications to understanding and treating this facet of the disease in humans.
<br />
<br />
<br />Cystic fibrosis is a fatal, genetic disease affecting 70,000 children and adults worldwide, and characterized by an overproduction of mucous in the lungs and digestive system. Compared to the 1960's, when most patients died by age four, the median age of survival is now 37 years.
<br />
<br />Rozmahel and his colleagues are identifying secondary genes that could contribute to CF, and measuring their impact on the disease. More specifically, they are investigating the potential of a gene found in mice, mCLCA3, which is similar to one in humans that exhibits abnormal levels in CF. The mCLCA3 gene is expressed by cells that produce and secrete mucous.
<br />
<br />The researchers discovered that mCLCA3 plays an important role in the property of mucous, thereby allowing it to be cleared rather than result in the blockages that underlie CF. By correcting the abnormal levels of mCLCA3 in CF mice they were able to overcome the mucous lesions.
<br />
<br />Whereas CF mice normally do not survive more than four weeks as a consequence of the mucous disease, the animals where mCLCA3 levels were corrected could live a normal lifespan.
<br />
<br />"It's my hope to understand what is causing the exaggerated mucous production and secretion in CF patients," says Dr. Rozmahel. "From there, we can figure out ways to correct it."
<br />
 

kitomd21

New member
Does it state how the levels we're corrected? Since we can't change our DNA (i.e., those already affected by CF), does this only apply to intro-type science?
 

kitomd21

New member
Does it state how the levels we're corrected? Since we can't change our DNA (i.e., those already affected by CF), does this only apply to intro-type science?
 

kitomd21

New member
Does it state how the levels we're corrected? Since we can't change our DNA (i.e., those already affected by CF), does this only apply to intro-type science?
 

kitomd21

New member
Does it state how the levels we're corrected? Since we can't change our DNA (i.e., those already affected by CF), does this only apply to intro-type science?
 

kitomd21

New member
Does it state how the levels we're corrected? Since we can't change our DNA (i.e., those already affected by CF), does this only apply to intro-type science?
 

Mommy2Alysa

New member
No it doesnt say anything about that but maybe because it is still in the testing stage they dont want to publish it?? Researchers are weird that way (worried about someone stealing their theories or methods so most dont share until it is already accepted for publication and such).

I think it may some sort of drug??? Not sure.
 

Mommy2Alysa

New member
No it doesnt say anything about that but maybe because it is still in the testing stage they dont want to publish it?? Researchers are weird that way (worried about someone stealing their theories or methods so most dont share until it is already accepted for publication and such).

I think it may some sort of drug??? Not sure.
 

Mommy2Alysa

New member
No it doesnt say anything about that but maybe because it is still in the testing stage they dont want to publish it?? Researchers are weird that way (worried about someone stealing their theories or methods so most dont share until it is already accepted for publication and such).

I think it may some sort of drug??? Not sure.
 

Mommy2Alysa

New member
No it doesnt say anything about that but maybe because it is still in the testing stage they dont want to publish it?? Researchers are weird that way (worried about someone stealing their theories or methods so most dont share until it is already accepted for publication and such).

I think it may some sort of drug??? Not sure.
 

Mommy2Alysa

New member
No it doesnt say anything about that but maybe because it is still in the testing stage they dont want to publish it?? Researchers are weird that way (worried about someone stealing their theories or methods so most dont share until it is already accepted for publication and such).
<br />
<br />I think it may some sort of drug??? Not sure.
 
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