Background-In patients with major trauma and burns, total enteral nutrition (TEN) significantly decreases the acute phase response and incidence of septic complications when compared with total parenteral nutrition (TPN). Poor outcome in acute pancreatitis is associated with a high incidence of systemic inflammatory response syndrome (SIRS) and sepsis. Aims-To determine whether TEN can attenuate the acute phase response and improve clinical disease severity in patients with acute pancreatitis. Methods-Glasgow score, Apache II, computed tomography (CT) scan score, C reactive protein (CRP), serum IgM antiendotoxin antibodies (EndoCAb), and total antioxidant capacity (TAC) were determined on admission in 34 patients with acute pancreatitis. Patients were stratified according to disease severity and randomised to receive either TPN or TEN for seven days and then re-evaluated. Results-SIRS, sepsis, organ failure, and ITU stay, were globally improved in the enterally fed patients. The acute phase response and disease severity scores were significantly improved following enteral nutrition (CRP: 156 (117-222) to 84 (50-141), p<0.005; APACHE II scores 8 (6-10) to 6 (4-8), p<0.0001) without change in the CT scan scores. In parenterally fed patients these parameters did not change but there was an increase in EndoCAb antibody levels and a fall in TAC. Enterally fed patients showed no change in the level of EndoCAb antibodies and an increase in TAC. Conclusion-TEN moderates the acute phase response, and improves disease severity and clinical outcome despite unchanged pancreatic injury on CT scan. Reduced systemic exposure to endotoxin and reduced oxidant stress also occurred in the TEN group. Enteral feeding modulates the inflammatory and sepsis response in acute pancreatitis and is clinically beneficial. (Gut 1998;42:431-435)

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The completion of the draft sequence of the rhesus macaque genome allowed us to study the genomic composition and evolution of transposable elements in this representative of the Old World monkey lineage, a group of diverse primates closely related to humans. The L1 family of long interspersed elements appears to have evolved as a single lineage, and Alu elements have evolved into four currently active lineages. We also found evidence of elevated horizontal transmissions of retroviruses and the absence of DNA transposon activity in the Old World monkey lineage. In addition,~100 precursors of composite SVA (short interspersed element, variable number of tandem repeat, and Alu) elements were identified, with the majority being shared by the common ancestor of humans and rhesus macaques. Mobile elements compose roughly 50% of primate genomes, and our findings illustrate their diversity and strong influence on genome evolution between closely related species.

Alu elements are primate-specific members of the SINE (short interspersed element) retroposon family, which comprise ∼10% of the human genome. Here we report the first chromosomal-level comparison examining the Alu retroposition dynamics following the divergence of humans and chimpanzees. We find a twofold increase in Alu insertions in humans in comparison to the common chimpanzee (Pan troglodytes). The genomic diversity (polymorphism for presence or absence of the Alu insertion) associated with these inserts indicates that, analogous to recent nucleotide diversity studies, the level of chimpanzee Alu diversity is ∼1.7 times higher than that of humans. Evolutionarily recent Alu subfamily structure differs markedly between the human and chimpanzee lineages, with the major human subfamilies remaining largely inactive in the chimpanzee lineage. We propose a population-based model to account for the observed fluctuation in Alu retroposition rates across primate taxa.[The sequence data from this study have been submitted to GenBank under accession nos. AY569161-AY569170.]Alu elements are primate-specific members of the SINE (short interspersed element) family of retroposons. They have enjoyed enormous success over the course of primate evolution and, by conservative estimates, comprise some 10% of the human genome (Schmid 1996;Lander et al. 2001). Largely as a result of the human genome project, a wealth of knowledge has been accumulated concerning the underlying biology, retroposition activity, and associated population genetics of Alu repeats (Schmid 1998;Batzer and Deininger 2002). The ubiquitous presence of Alu sequences within primate genomes has been the cumulative result of a "copy and paste" mechanism, in which an RNA polymerase III-generated transcript is reverse-transcribed and integrated into the genome (Burke et al. 1999). In addition to being wholly dependent upon host cellular processes for their transmission through the germline, Alu elements also lack the ability to generate the endonuclease and reverse transcriptase necessary for their own retroposition. Instead, they must appropriate the necessary enzymatic machinery from L1, a member of the LINE (long interspersed element) retroposon family (Jurka 1997;Kajikawa and Okada 2002). As a result of this obligatory relationship with their genomic host and other transposable elements, the Alu family has been characterized as a "parasite's parasite" (Schmid 2003). Despite the family's various designations as "junk," "parasites," and "selfish DNA," researchers have been reluctant to dismiss them as entirely self-serving genomic entities. A number of investigators have suggested a potential role for Alu elements within their host genomes, and recent implications of Alu element involvement in alternative splicing, segmental duplications, and DNA repair serve to further fuel these arguments (Morrish et al. 2002;Bailey et al. 2003;Lev-Maor et al. 2003;Salem et al. 2003a). Whether these observations constitute adaptations, exaptations (i.e., they have been comma...