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Untitled - D Ank Unlimited

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endotoxin shock 249 envelope glycoprotein (Env)<br />

endotoxin shock<br />

Circulatory and metabolic collapse following exposure to<br />

excessive quantities of cytokines, especially IL1 and TNF,<br />

introduced into the blood circulation by macrophages following<br />

Gram-negative bacterial infection or their products<br />

such as lipopolysaccharide. Falling blood pressure and<br />

disseminated intravascular coagulation (DIC) following<br />

exposure to relatively large amounts of endotoxin<br />

produced during bacterial sepsis with Escherichia coli,<br />

Pseudomonas aeruginosa, or meningococci. DIC leads to<br />

the formation of thrombi in small blood vessels and such<br />

devastating consequences as bilateral cortical necrosis of<br />

the kidneys and blockage of the blood supply to the brain,<br />

lungs, and adrenals. When DIC affects the adrenal glands,<br />

as in certain meningococcal infections, infarction leads to<br />

adrenal insufficiency and death. This is the Waterhouse–<br />

Friderichsen syndrome. Referred to also as septic shock.<br />

engraftment<br />

The phase during which transplanted bone marrow manufactures<br />

new blood cells.<br />

enhancement<br />

The prolonged survival (or, conversely, the delayed rejection)<br />

of tumor or skin allografts in individuals previously<br />

immunized or conditioned by passive injection of antibody<br />

specific for graft antigens. This is termed immunological<br />

enhancement and is believed to be due to a blocking effect<br />

by the antibody.<br />

enhanceosome<br />

A multiprotein transactivator complex that unites with an<br />

active promoter to initiate or facilitate gene transcription.<br />

Refer to SXY-CIITA regulatory system.<br />

enhancer<br />

A segment of DNA containing a group of DNA-binding<br />

motifs that can elevate the amount of RNA a cell produces.<br />

This DNA sequence activates the beginning of RNA polymerase<br />

II transcription from a promoter. Although initially<br />

described in the SV40 DNA tumor virus, enhancers have<br />

now been demonstrated in the J–C introns of immunoglobulin<br />

μ and κ genes. Immunoglobulin enhancers function<br />

well in B cells, presumably due to precise regulatory<br />

proteins that communicate with the enhancer region.<br />

enhancing antibodies<br />

Blocking antibodies that favor survival of tumor or normal<br />

tissue allografts.<br />

enkephalins<br />

A related group of endogenous opioids that are pentamers<br />

synthesized in the central nervous system and gastrointestinal<br />

tract. They share the initial four amino acids<br />

(H–Tyr–Gly–Gly–Phe).<br />

entactin/nidogen<br />

Glomerular basement membrane antigens that may have<br />

a possible role in glomerular basement membrane nephritis.<br />

Entactin is a 150-kDa glomerular membrane-sulfated<br />

glycoprotein that is probably synthesized by endothelial and<br />

epithelial cells in the developing kidney. It has a role in cellular<br />

adhesion to extracellular material. It is complexed with<br />

laminin in vivo. Nidogen, also a basement membrane constitutent,<br />

is a 150-kDa glycoprotein that has binding affinity for<br />

laminin. Entactin and nidogen closely resemble one another<br />

and may be identical. In one study, serum IgG, IgM, and/or<br />

IgA antibodies specific for entactin/nidogen were found in<br />

more than 40% of patients with glomerulonephritis.<br />

entactin/nidogen autoantibodies<br />

Autoantibodies against entactin, a 150-kDa sulfated<br />

glycoprotein present in the glomerular plasma membrane.<br />

Entactin is believed to be synthesized by endothelial and<br />

epithelial cells in the developing kidney, but in the mature<br />

tissue. It is believed to play a role in cellular adhesion<br />

to extracellular material. Laminin and entactin form a<br />

complex in vivo. Nidogen, another sulfated glycoprotein,<br />

was identified in the basement membrane matrix of EHS<br />

sarcoma. Nidogen is a 150-kDa glycoprotein and, similar<br />

to entactin, reveals an in vitro binding affinity for laminin.<br />

Subsequent investigations have shown nidogen and entactin<br />

to be similar or identical. More than 40% of 206 patients<br />

with glomerulonephritis develop immunoglobulin G (IgG),<br />

IgM, and/or IgA autoantibodies against entactin/nidogen.<br />

Entactin autoantibodies of IgG, IgA, and IgM classes have<br />

been found in the sera of system lupus erythematosus (SLE)<br />

patients, but IgA entactin autoantibodies are found most<br />

frequently in patients with IgA nephropathy.<br />

Entamoeba histolytica antibody<br />

Specific serum antibody that develops in essentially all<br />

individuals infected with E. histolytica. The antibody<br />

responses are composed mainly of immunoglobulin G<br />

(IgG) and to a lesser degree IgA. IgM declines quickly,<br />

whereas specific IgG remains increased for months or<br />

years. Coproantibodies are found in the feces of patients<br />

with amebic dysentery, whereas patients with amebic liver<br />

abscesses have secretory IgA in their saliva and colostrum.<br />

There is little evidence of cellular immunity and granuloma<br />

formation in flemebic dysentery ulcers and in amebic liver<br />

abscesses. E. histolytica trophozoites not only resist normal<br />

human leukocytes but in fact kill them. Interferon γ (IFN-γ)<br />

induced by antigenic stimulation activates macrophages<br />

to kill trophozoites. The organism is potently chemotactic<br />

for neutrophils that are killed on contact with the parasite.<br />

Lytic enzymes released from dead cells induce tissue injury.<br />

IFN-γ- and TNF-α-activated neutrophils are able to kill<br />

trophozoites. There have been conflicting reports of the<br />

relative complement sensitivity of E. histolytica.<br />

enteric neuronal autoantibodies<br />

Immunoglobulin G (IgG) autoantibodies that react strongly<br />

with nuclei and weakly with cytoplasm of enteric nuclei<br />

of myenteric and submucosal plexuses. They develop in<br />

selected patients with the paraneoplastic syndrome marked<br />

by intestinal pseudo-obstruction in association with small<br />

cell lung carcinoma. These autoantibodies are nonreactive<br />

with nuclei of non-neuronal tissue. Myenteric neuronal<br />

autoantibodies are specific for enteric neuronal neurofilaments,<br />

and they can be detected in scleroderma and visceral<br />

neuropathy patients.<br />

enterocytes<br />

Intestinal epithelial cells that actively imbibe nutrients.<br />

They bear Toll-like receptors and synthesize cytokines that<br />

facilitate intestinal intraepithelial lymphocyte activation.<br />

enterotoxin<br />

A heat-stable bacterial toxin that causes intestinal injury.<br />

envelope<br />

Phospholipid bilayer that encircles a viral core. For example,<br />

the HIV-1 viral envelope expresses gp41 and gp120.<br />

envelope glycoprotein (Env)<br />

A gene of retroviruses that codes for env envelope glycoprotein<br />

(refer to HIV-1 genes). It is present on the plasma<br />

E

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