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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."
 
M

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."
 
M

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."
 
M

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."
 
M

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 />
 
M

Mommy2Alysa

New member
there is another one from the city paper today

London scientists working with mice have discovered that by correcting an abnormal gene linked to cystic fibrosis the mouse has a normal two-year lifespan instead of dying at four or six weeks.

The hope is the research will eventually lead to a new treatment for the fatal genetic disorder that hits one in 3,600 Canadians.

"The important aspect of this will be the translation of this research from the mouse model back into the clinical setting into actual cystic fibrosis patients," said Dr. Richard Rozmahel of the Lawson Research Institute.

Rozmahel's research team looked at more than 30,000 genes to find ones different in a normal mouse from one in cystic fibrosis mice.

One gene with a different expression in cystic fibrosis mice was mCLCA3, a gene similar to one found in humans with cystic fibrosis.

In the CF mice, it was only being expressed at one-third the level of healthy mice.

When the Lawson scientists brought the gene up to normal expression, the mucous blockages in the lungs and intestines were reduced.

"They could survive normally," said Rozmahel.

The next step in their research will be to pinpoint exactly how the gene CLCA3 functions, he said.

"We have shown CLCA3 is important to cystic fibrosis but the function of CLCA3 is not fully understood," said Rozmahel.

"Is it acting on the properties of the mucous to allow the mucous to be cleared better, is it working on the hydration of the mucous so that mucous has more fluid in it so it would be cleared better, or is it acting to decrease secretion of the mucous by these cells?"

Individuals born with cystic fibrosis used to survive only a few years, but drug therapies and lung transplants have pushed the median life expectancy to 37.

The most obvious problem for individuals with the disease is the build of mucous in the lungs, which provides a breeding ground for bacteria.

"In cystic fibrosis the mucous is not able to be cleared because it is so thick and sticky," Rozmahel said.

"If we were able to promote the clearance of mucous we would be able to correct at least part of the problem."
 
M

Mommy2Alysa

New member
there is another one from the city paper today

London scientists working with mice have discovered that by correcting an abnormal gene linked to cystic fibrosis the mouse has a normal two-year lifespan instead of dying at four or six weeks.

The hope is the research will eventually lead to a new treatment for the fatal genetic disorder that hits one in 3,600 Canadians.

"The important aspect of this will be the translation of this research from the mouse model back into the clinical setting into actual cystic fibrosis patients," said Dr. Richard Rozmahel of the Lawson Research Institute.

Rozmahel's research team looked at more than 30,000 genes to find ones different in a normal mouse from one in cystic fibrosis mice.

One gene with a different expression in cystic fibrosis mice was mCLCA3, a gene similar to one found in humans with cystic fibrosis.

In the CF mice, it was only being expressed at one-third the level of healthy mice.

When the Lawson scientists brought the gene up to normal expression, the mucous blockages in the lungs and intestines were reduced.

"They could survive normally," said Rozmahel.

The next step in their research will be to pinpoint exactly how the gene CLCA3 functions, he said.

"We have shown CLCA3 is important to cystic fibrosis but the function of CLCA3 is not fully understood," said Rozmahel.

"Is it acting on the properties of the mucous to allow the mucous to be cleared better, is it working on the hydration of the mucous so that mucous has more fluid in it so it would be cleared better, or is it acting to decrease secretion of the mucous by these cells?"

Individuals born with cystic fibrosis used to survive only a few years, but drug therapies and lung transplants have pushed the median life expectancy to 37.

The most obvious problem for individuals with the disease is the build of mucous in the lungs, which provides a breeding ground for bacteria.

"In cystic fibrosis the mucous is not able to be cleared because it is so thick and sticky," Rozmahel said.

"If we were able to promote the clearance of mucous we would be able to correct at least part of the problem."
 
M

Mommy2Alysa

New member
there is another one from the city paper today

London scientists working with mice have discovered that by correcting an abnormal gene linked to cystic fibrosis the mouse has a normal two-year lifespan instead of dying at four or six weeks.

The hope is the research will eventually lead to a new treatment for the fatal genetic disorder that hits one in 3,600 Canadians.

"The important aspect of this will be the translation of this research from the mouse model back into the clinical setting into actual cystic fibrosis patients," said Dr. Richard Rozmahel of the Lawson Research Institute.

Rozmahel's research team looked at more than 30,000 genes to find ones different in a normal mouse from one in cystic fibrosis mice.

One gene with a different expression in cystic fibrosis mice was mCLCA3, a gene similar to one found in humans with cystic fibrosis.

In the CF mice, it was only being expressed at one-third the level of healthy mice.

When the Lawson scientists brought the gene up to normal expression, the mucous blockages in the lungs and intestines were reduced.

"They could survive normally," said Rozmahel.

The next step in their research will be to pinpoint exactly how the gene CLCA3 functions, he said.

"We have shown CLCA3 is important to cystic fibrosis but the function of CLCA3 is not fully understood," said Rozmahel.

"Is it acting on the properties of the mucous to allow the mucous to be cleared better, is it working on the hydration of the mucous so that mucous has more fluid in it so it would be cleared better, or is it acting to decrease secretion of the mucous by these cells?"

Individuals born with cystic fibrosis used to survive only a few years, but drug therapies and lung transplants have pushed the median life expectancy to 37.

The most obvious problem for individuals with the disease is the build of mucous in the lungs, which provides a breeding ground for bacteria.

"In cystic fibrosis the mucous is not able to be cleared because it is so thick and sticky," Rozmahel said.

"If we were able to promote the clearance of mucous we would be able to correct at least part of the problem."
 
M

Mommy2Alysa

New member
there is another one from the city paper today

London scientists working with mice have discovered that by correcting an abnormal gene linked to cystic fibrosis the mouse has a normal two-year lifespan instead of dying at four or six weeks.

The hope is the research will eventually lead to a new treatment for the fatal genetic disorder that hits one in 3,600 Canadians.

"The important aspect of this will be the translation of this research from the mouse model back into the clinical setting into actual cystic fibrosis patients," said Dr. Richard Rozmahel of the Lawson Research Institute.

Rozmahel's research team looked at more than 30,000 genes to find ones different in a normal mouse from one in cystic fibrosis mice.

One gene with a different expression in cystic fibrosis mice was mCLCA3, a gene similar to one found in humans with cystic fibrosis.

In the CF mice, it was only being expressed at one-third the level of healthy mice.

When the Lawson scientists brought the gene up to normal expression, the mucous blockages in the lungs and intestines were reduced.

"They could survive normally," said Rozmahel.

The next step in their research will be to pinpoint exactly how the gene CLCA3 functions, he said.

"We have shown CLCA3 is important to cystic fibrosis but the function of CLCA3 is not fully understood," said Rozmahel.

"Is it acting on the properties of the mucous to allow the mucous to be cleared better, is it working on the hydration of the mucous so that mucous has more fluid in it so it would be cleared better, or is it acting to decrease secretion of the mucous by these cells?"

Individuals born with cystic fibrosis used to survive only a few years, but drug therapies and lung transplants have pushed the median life expectancy to 37.

The most obvious problem for individuals with the disease is the build of mucous in the lungs, which provides a breeding ground for bacteria.

"In cystic fibrosis the mucous is not able to be cleared because it is so thick and sticky," Rozmahel said.

"If we were able to promote the clearance of mucous we would be able to correct at least part of the problem."
 
M

Mommy2Alysa

New member
there is another one from the city paper today
<br />
<br />London scientists working with mice have discovered that by correcting an abnormal gene linked to cystic fibrosis the mouse has a normal two-year lifespan instead of dying at four or six weeks.
<br />
<br />The hope is the research will eventually lead to a new treatment for the fatal genetic disorder that hits one in 3,600 Canadians.
<br />
<br />"The important aspect of this will be the translation of this research from the mouse model back into the clinical setting into actual cystic fibrosis patients," said Dr. Richard Rozmahel of the Lawson Research Institute.
<br />
<br />Rozmahel's research team looked at more than 30,000 genes to find ones different in a normal mouse from one in cystic fibrosis mice.
<br />
<br />One gene with a different expression in cystic fibrosis mice was mCLCA3, a gene similar to one found in humans with cystic fibrosis.
<br />
<br />In the CF mice, it was only being expressed at one-third the level of healthy mice.
<br />
<br />When the Lawson scientists brought the gene up to normal expression, the mucous blockages in the lungs and intestines were reduced.
<br />
<br />"They could survive normally," said Rozmahel.
<br />
<br />The next step in their research will be to pinpoint exactly how the gene CLCA3 functions, he said.
<br />
<br />"We have shown CLCA3 is important to cystic fibrosis but the function of CLCA3 is not fully understood," said Rozmahel.
<br />
<br />"Is it acting on the properties of the mucous to allow the mucous to be cleared better, is it working on the hydration of the mucous so that mucous has more fluid in it so it would be cleared better, or is it acting to decrease secretion of the mucous by these cells?"
<br />
<br />Individuals born with cystic fibrosis used to survive only a few years, but drug therapies and lung transplants have pushed the median life expectancy to 37.
<br />
<br />The most obvious problem for individuals with the disease is the build of mucous in the lungs, which provides a breeding ground for bacteria.
<br />
<br />"In cystic fibrosis the mucous is not able to be cleared because it is so thick and sticky," Rozmahel said.
<br />
<br />"If we were able to promote the clearance of mucous we would be able to correct at least part of the problem."
<br />
<br />
 
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