Three deer from
the heart of spring-
thin as paper,
wide as the woods-
remind me of
our three hearts,
and what i give up
being unreasonable
or mean-spirited.
Heart is renewal,
willing to call out
to that which doesn't
yet know love,
letting it run along
with running deer
thru impossible thickets,
white tails fluffed
to the sky,
opening deer eyes
in eternity.
Wednesday, March 31
Saturday, March 13
Friday, March 5
Thursday, March 4
Chip
The chip on
our shoulder
is the stone
blocking the
entrance to
the cave of
our own heart
our shoulder
is the stone
blocking the
entrance to
the cave of
our own heart
Labels:
poems: a-e
Tuesday, March 2
Alpha-1 Antitrypsin Deficiency
Alpha-1 Antitrypsin Deficiency is a rare genetic condition in which levels of Alpha-1 Antitrypsin (AAT), a protein produced in the liver and crucial to healthy lungs, are insufficient to perform their normal function. This protein's role is to neutralize/shut down defensive enzymes in the lungs as needed during routine maintenance or as defensive "battles" in the lungs progress. Deficient in this critical protein, the enzymes remain unchecked and, even when the threatening "event" is over, continue attacking the only target left: healthy lung tissue, resulting in "genetic" emphysema.
"It is now known that the low circulating levels of AAT in Alpha-1 are due to abnormal folding of the defective AAT in the endoplasmic reticulum of the liver leading to polymerization and accumulation of AAT in hepatocytes. Since the liver is the primary source of circulating AAT, this accounts for the decreased circulating levels of this important protein. The accumulation of polymerized abnormal protein in the hepatocytes appears to be the cause of the increased risk of cirrhosis and liver failure in individuals with Alpha-1."
Alpha-1 Antitrypsin Deficiency was discovered in 1963 by Carl-Bertil Laurel at the University of Lund in Sweden, along with a medical resident, Sten Eriksson. A link with liver disease was established in 1969. A1AD is most common among people of Northern Europe descent. There is some belief that "A1AD originated in Scandinavia and during the Viking exploration was spread throughout northern and eastern Europe".
There is only one known therapy, an infusion done on a weekly, bi-weekly, or monthly basis, that can temporarily slow the progression of the disease. Organ transplants are the last resort.
Links:
Alpha-1 Association
Alpha-1 Foundation
Medline Plus: Alpha-1 Antitrypsin Deficiency
Genetics Home Reference: Alpha-1 Antitrypsin Deficiency
National Human Genome Research Institute
Alpha-1 Antitrypsin Deficiency Research Database
"It is now known that the low circulating levels of AAT in Alpha-1 are due to abnormal folding of the defective AAT in the endoplasmic reticulum of the liver leading to polymerization and accumulation of AAT in hepatocytes. Since the liver is the primary source of circulating AAT, this accounts for the decreased circulating levels of this important protein. The accumulation of polymerized abnormal protein in the hepatocytes appears to be the cause of the increased risk of cirrhosis and liver failure in individuals with Alpha-1."
Alpha-1 Antitrypsin Deficiency was discovered in 1963 by Carl-Bertil Laurel at the University of Lund in Sweden, along with a medical resident, Sten Eriksson. A link with liver disease was established in 1969. A1AD is most common among people of Northern Europe descent. There is some belief that "A1AD originated in Scandinavia and during the Viking exploration was spread throughout northern and eastern Europe".
There is only one known therapy, an infusion done on a weekly, bi-weekly, or monthly basis, that can temporarily slow the progression of the disease. Organ transplants are the last resort.
Links:
Alpha-1 Association
Alpha-1 Foundation
Medline Plus: Alpha-1 Antitrypsin Deficiency
Genetics Home Reference: Alpha-1 Antitrypsin Deficiency
National Human Genome Research Institute
Alpha-1 Antitrypsin Deficiency Research Database
Subscribe to:
Posts (Atom)