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2 s, only 3 cases were clinically diagnosed as amoebic appendicitis, including 2 diagnosed at the time
9 ne proteinases are a key virulence factor in amoebic colitis, and provide a novel mechanism for their
10 cysteine proteinases in the pathogenesis of amoebic colitis, human intestinal xenografts in SCID mic
14 results demonstrate for the first time that amoebic cysteine proteinases are a key virulence factor
18 amage may be explained by our discovery that amoebic cysteine proteinases possess IL-1B converting en
20 ntamoeba histolytica, the causative agent of amoebic dysentery, was determined to have raft-like plas
21 rtunistic pathogen that causes granulomatous amoebic encephalitis (GAE), a chronic and often fatal di
22 meningoencephalitis, a chronic granulomatous amoebic encephalitis (GAE), and a chronic amoebic kerati
24 simple, reliable, and reproducible method of amoebic enumeration that depends on simply establishing
26 occurred early, because the sequences of the amoebic enzymes show considerable divergence from those
27 ivergence from those of prokaryotes, and the amoebic genes encoding these enzymes are in the AT-rich
28 ograms to analyze the promoter regions of 57 amoebic genes that had increased expression specifically
38 owleri is known to cause the disease primary amoebic meningoencephalitis (PAM) and can be found in dr
39 mparatively low levels of infection, primary amoebic meningoencephalitis (PAM) induced by Naegleria f
42 t both Acanthamoeba trophozoites and soluble amoebic products induce an early anti-inflammatory monoc
43 , nibble) observed between immune cells, but amoebic trogocytosis differs because it results in death
47 ytica infection have begun to illuminate how amoebic trophozoites cause intestinal disease and liver
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