Untitled - D Ank Unlimited

levamisole 450 Levine, Philip
Philip Levine.
Le
(Le x )
Le a
(Le x )
Type 1 precursor
β1, 3
Se
R (H)
(β1, 4)
(Type 2 precursor)
se
(h)
R
Le
D-galactose
(Le y )
Type 1H
Le b
(Le y )
(Type 2H)
R
N-acetyl-D-glucosamine
R
R
A
O
B
of cells. Most cells synthesize plentiful amounts of leukotriene
C (LTC) and its breakdown products, LTD and LTE,
which bind to smooth muscle cell receptors to produce prolonged
bronchoconstriction. Leukotrienes play a significant
role in the pathogenesis of bronchial asthma. The former
SRS-A term covered the collective actions of LTD and
LTE. Refer also to arachidonic acid (AA) and leukotrienes.
levamisole
An antihelminthic drug used extensively in domestic animals
and birds that was found to also produce immunostimulant
effects. It may potentiate or restore the functions of T lymphocytes
and other leukocytes. It increases the magnitude of
delayed-type hypersensitivity or T-cell-medicated immunity
in humans. It has some efficacy in the treatment of rheumatoid
arthritis and induces severe agranular cytosis, which
requires discontinuation of use. It also potentiates the action
of fluorouracil in adjuvant therapy of colorectal cancer.
Levine, Philip
Russian–American immunohematologist. With
Landsteiner, he conducted pioneering research on blood
group antigens, including discovery of the MNP system.
His work contributed much to transfusion medicine and
transplantation immunobiology.
A
A
B
Le
(Le x )
le
R
R
Le
le
Le
le
le
(Le x )
(Le x )
Le
R (Lex )
L-fucose in α1 2 linkage
L-fucose in α1 3 (or α1 4) linkage
N-acetyl-D-galactosamine R Remainder of molecule
Biosynthetic pathways of ABH, Lewis, and XY antigens derived from type I and type II core chains. Genes controlling steps in the pathway are shown in
italics. Types I and II precursors differ in the nature of the linkage between the nonreducing terminal galactolose and N-acetylglucosamine: β 1–3 in type
I and β 1–4 in type II. Type II structures and the genes that act on them are shown in parentheses. Dashed lines show how Le a and (Le x )Le d (Le y ), produced
from the precursor and H structures, respectively, are not substrates for the H, Se, or ABO transferases and remain unconverted.
A
A
R
R
R
R
R
R
R
R
ALe b
(ALe y )
A
Leb
(Le y )
H
BLe b
(BLe y )
B
Le a
(Le x )