Untitled - D Ank Unlimited

Feulgen reaction 271 fibrin
villous cytotrophoblasts and syncytiotrophoblasts any
classical polymorphic histocompatibility complex (MHC)
class I or II antigens. Constitutive human leukocyte antigen
(HLA) expression is also not induced by known upregulators
such as interferon-γ. Thus, classical MHC antigens are
not expressed throughout gestation. Extravillous cytotrophoblast
cells selectively express HLA-G, a nonclassical
MHC class I antigen that has limited genetic polymorphism.
HLA-G may protect the cytotrophoblast population from
MHC-nonrestricted natural killer (NK) cell attack. The
trophoblast also protects itself from maternal cytotoxicity
during gestation by expressing a high level of complement
regulatory proteins on its surface such as membrane cofactor
protein (MCP; CD46), decay-accelerating factor (DAF;
CD55), and membrane attack complex inhibitory factor
(CD59). The maternal immune system recognizes pregnancy
(i.e., the fetal trophoblast) in a manner that results in cellular,
antibody, and cytokine responses that protect the fetal
allograft. CD56-positive large granular lymphocytes may be
regulated by hormones in the endometrium that control their
function. They have been suggested to be a form of NK cell
in arrested maturation, possibly due to persistent expression
of HLA-G on target invasive cytotrophoblast. Contemporary
studies have addressed cytokine interactions at the fetal–
maternal tissue interface in pregnancy. HLA-G or other fetal
trophoblast antigens have been postulated to possibly stimulate
maternal lymphocytes in endometrial tissue to synthesize
cytokines and growth factors that act in a paracrine
manner beneficial to trophoblast growth and differentiation.
This has been called the immunotrophism hypothesis. Other
cytokines released into decidual tissue include colonystimulating
factors (CSFs), tumor necrosis factor α (TNF-α),
IL6, and transforming growth factor β (TGF-β). Fetal
syncytiotrophoblast has numerous growth factor receptors.
Thus, an extensive cytokine network is present within the
uteroplacental tissue that offers both immunosuppressive
and growth-promoting signals. In humans, IgG is selectively
transported across the placenta into the fetal circulation
following combination with transporting Fcγ receptors on
the placenta. This transfer takes place during the 20th to the
22nd week of gestation. Maternal HLA-specific alloantibody
that is specific for the fetal HLA type is bound by nontrophoblastic
cells expressing fetal HLA antigens, including
macrophages, fibroblasts, and endothelium within the villous
mesenchyme of placental tissue, thereby preventing these
antibodies from reaching the fetal circulation. Maternal antibodies
against any other antigen of the fetus will likewise be
bound within the placental tissues to a cell expressing that
antigen. The placenta acts as a sponge to absorb potentially
harmful antibodies. Exceptions to placental trapping of
deleterious maternal IgG antibodies include maternal IgG
antibodies against RhD antigen and certain maternal organspecific
autoantibodies.
Feulgen reaction
A standard method that detects DNA in tissues.
fever
An increase in the body temperature above normal.
Attributable to cytokines released during infection.
fibrillarin antibodies
Antibodies against fibrillarin found in about 8% of patients
with diffuse and limited scleroderma. Fibrillarin is a 34-kDa
protein constituent of U3 ribonucleoprotein (U3-RNP).
Mercuric chloride induces autoantibodies against U3 small
nuclear ribonucleoprotein in susceptible mice.
fibrillarin autoantibodies
Antibodies discovered in 4 to 9% of patients with scleroderma.
Fibrillarin is the main 34-kDa component of U3
ribonucleoprotein (U3-RNP). Fifty-six percent of black
patients with diffuse cutaneous scleroderma compared
with only 14% of black patients with limited cutaneous
scleroderma and white patients with diffuse and limited
cutaneous scleroderma (5% and 4%, respectively) had antifibrillarin
autoantibodies in their sera. Mercuric chloride can
induce fibrillarin antibodies in mouse strains that recognize
the same epitopes as fibrillarin antibodies found in scleroderma
patients and are mainly of the immunoglobulin G
(IgG) class. The demonstration that selected human leukocyte
antigen (HLA) haplotypes occur at a greater frequency
in patients with fibrillarin antibodies suggests a genetic
predisposition to develop these autoantibodies. Indirect
immunofluorescence and immunoblotting are the methods
of choice for antifibrillarin antibody detection.
fibrin
Fibrinogen
Thrombin
H 2 O Fibrinopeptides
Fibrin Soft Clot
Fibrin.
Fibrin
Protein responsible for the coagulation of blood. It is
formed through the degradation of fibrinogen into fibrin
monomers. Polymerization of the nascent fibrin molecules
(comprising the α, β, and γ chains) occurs by end-to-end as
well as lateral interactions. The fibrin polymer is envisaged
as having two chains of the triad structure lying side by
side in a staggered fashion in such a way that two terminal
nodules are associated with the central nodule of a third
molecule. The chains may also be twisted around each
other. The fibrin polymer thus formed is stabilized under
the action of a fibrin-stabilizing factor, another component
of the coagulation system. Fibrinogen may also be degraded
by plasmin. In this process, a number of intermediates,
designated as fragments X, Y, D, and E, are formed. These
fragments interfere with polymerization of fibrin by binding
to nascent intact fibrin molecules, thus causing a defective
and unstable polymerization. Fibrin is also cleaved by plasmin
into similar but shorter fragments, collectively designated
fibrin degradation products. Of course, any excess of
such fragments will impair the normal coagulation process,
F