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Abstract

Self-propelled vehicles are those automobiles motorcycles aircraft, boats, snowmobiles, trucks, tractors jet skis, lawn mowers, golfcarts, etc., that convert their own energy supply into motive power used for propulsion. Batteries do so by converting electrochemical energy; engines do so by burning fuels to release their chemical energy. The majority of this equipment uses internal combustion engines such as a jet, diesel, or gasoline engines that consume flammable gases or liquids. Machinery may also employ engines to do other work such as turning crankshafts or generating electricity. External combustion engines include the steam engine which burns fuel to heat water, which on conversion to steam provides motive force.

Self-propelled vehicles automobiles motorcycles tractors engines
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49CFR.
Title 49-Transportation, Code of Federal Regulations; Office of the Federal Register, U.S. National Archives and Records Administration, Revised as of Oct 1, 1998 as amended by Federal Registers through January 31, 1999 Google Scholar
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,8th Edition; McGraw-Hill: New York, 1997 Google Scholar
©Springer-Verlag Berlin Heidelberg1999

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We further investigated the gene expression profiles through transcriptome sequencing of 29 EATL tumors for which RNA was available, including type I ( n = 16) and type II ( n = 13) cases. Unbiased principal-component analysis revealed that a large amount of variation in the gene expression data are driven by the differences between type I and type II cases. Plotting each of the EATL samples in the principal component space ( Fig. 2 c ) shows that the majority of samples segregate into the two groups corresponding essentially to the EATL subtypes, indicating robust differences in gene expression levels between the two subtypes. Based on these findings, we performed supervised differential expression analysis using the clinically derived labels of type I and type II. Fig. 2 d shows the genes that were at least 1.5-fold differentially expressed between the two types, with a false discovery rate of less than 0.1. Some notable genes with higher expression in the type I cases, compared with type II, included STAT3 , STAT5A , IRF1 , and IRF4 . The genes FASLG , SYK , and TGBR1 were found to be more highly expressed in type II EATL than in type I. Transglutaminase 2 ( TGM2 ) is an important enzyme and autoantigen in celiac disease ( Dieterich et al., 1997 ), which we found to be expressed at higher levels in the type I cases than in type II cases. NCAM1 , also known as CD56, was expressed higher in type II EATL, consistent with the use of CD56 staining as a diagnostic feature of type II EATL. We did not find MYC to be differentially expressed, despite the higher proportion of chromosome 8q amplifications in type II. The full list of differentially expressed genes is included in Table S6.

Fig. 2 e depicts the heat map of the differentially expressed genes in the 29 EATL samples, along with HLA genotype and celiac disease status. With a false discovery rate (FDR) <0.1 and a fold change of at least 1.5× in either direction, 380 genes are higher in type II and 198 genes are higher in type I. The cluster assignment, based on consensus K-means clustering of the differentially expressed genes, was found to track very closely with the original clinical EATL subtype.

Gene set enrichment of the differentially expressed genes revealed significant overexpression of the interferon-γ signaling pathway (P < 0.001; Fig. 2, f and g ) in type I EATLs. Genes expressed higher in type II EATL were found to be enriched for the natural killer-like cytotoxicity pathway (P = 0.02; Fig. 2, h and i ). Both interferon-γ signaling and natural killer–like cytotoxicity ( Wiki Cheap Online Countdown Package Dondup gradient longsleeve sweater Sale Best Prices ZoymNsb1z1
) are known functions of intraepithelial lymphocytes (IELs), which are the presumed cell of origin for EATLs ( Ebert, 1990 ; Taguchi et al., 1991 ; Ishikawa et al., 1993 ; Kagnoff, 1998 ; Corazza et al., 2000 ). Increased interferon-γ production has been described in patients with untreated celiac disease, consistent with the higher expression of this function in celiac-associated type I EATL ( Kagnoff, 1998 ; Nilsen et al., 1998 ). Other enriched gene sets of interest included MAPK signaling, up-regulated in type II, consistent with a previous study of high MAPK protein expression in type II ( Kikuma et al., 2014 ).

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