The normal LV differs in volume and mass between sexes and among certain ethnic groups. When indexed by body surface area, LV mass was independent of age for both sexes. Studies that assess cardiovascular risk factors in relationship to cardiac function and structure need to account for these normal variations in the population.

In this cohort free of clinical cardiovascular disease, modifiable risk factors were associated with subclinical alterations in LV size and systolic function as detected by cardiac MRI.

In Vibrio cholerae, the genes encoding cholera toxin (ctxAB) are located on a segment of DNA (termed the "core" region) that is flanked by two or more copies of a repeated sequence called RS1. Together these DNA units comprise the CTX genetic element. Evidence presented here suggests that RS1 sequences encode a site-specific recombination system, which allows integration of a suicide plasmid carrying RS1 into an 18-base-pair sequence (attRSl) located on the chromosome of nontoxigenic V. cholera" strains. Strains of V. cholerae with large deletions removing attRSl and the entire CTX genetic element no longer undergo site-specific recombination with the RS1 sequence. Additionally, these deletion strains show a defect in intestinal colonization. Recombination experiments localize the gene responsible for enhancing colonization to a portion of the core region of the CTX element. The identifled gene encodes a peptide that is highly similar in amino acid sequence to the flexible pilin of Aeromonas hydrophia. These results have important implications in the construction of stable, live attenuated cholera vaccines.The bacterium Vibrio cholerae is the causative agent of cholera, a diarrheal disease that has recently caused an explosive epidemic in Latin America (1). Although this organism has been studied for over 100 years, there still remains a need for an effective cholera vaccine. Recent efforts in developing live attenuated vaccines have focused on the construction of recombinant V. cholerae strains lacking the gene (ctxA) encoding the active subunit of cholera toxin (2-5). Since recombination with wild-type strains could restore toxigenicity to ctxA deletion strains, recA mutations have been examined as a means of stabilizing such live vaccine candidates (6, 7). Naturally occurring strains of V. cholerae that carry duplications of the ctx genes also have duplications of flanking DNA sequences, whereas nontoxigenic strains lack both ctx genes and flanking sequences (2, 8, 9). These observations suggest that the toxin genes are part of a larger genetic element (2,8,9). In V. cholerae strains of the El Tor biotype, this genetic element has been found to consist of a "core" region, which carries the ctxAB operon (10) and the zot gene encoding zona occludens toxin (11), flanked by two or more copies of a 2.7-kb repetitive sequence called RS1. Thus, the ctx genetic element is structurally analogous to compound transposons such as Tn9 (12) with RS1 sequences corresponding to ISJ insertion sequences directly duplicated at the termini. Unlike most transposons, the ctx genetic element appears to be located at the same chromosomal site in all El Tor strains (8), suggesting it may display a high degree of insertion site specificity, as do transposons Tn7 (13) and TnS54 (14).In this paper we show that the RS1 sequences associated with the CTX genetic element apparently mediate recAindependent site-specific recombination between the element and an 18-bp target site on the V. cholerae chromosome called attRS1. In addition...

SummaryCTX is a filamentous phage that encodes cholera toxin, one of the principal virulence factors of Vibrio cholerae. CTX is unusual among filamentous phages because it can either replicate as a plasmid or integrate into the V. cholerae chromosome at a specific site. The CTX genome has two regions, the 'core' and RS2. Integrated CTX is frequently flanked by an element known as RS1 which is related to RS2. The nucleotide sequences of RS2 and RS1 were determined. These related elements contain three nearly identical open reading frames (ORFs), which in RS2 were designated rstR, rstA2 and rstB2. RS1 contains an additional ORF designated rstC. Functional analyses indicate that rstA2 is required for CTX replication and rstB2 is required for CTX integration. The amino terminus of RstR is similar to the amino termini of other phageencoded repressors, and RstR represses the expression of rstA2. Although genes with related functions are clustered in the genome of CTX in a way similar to those for other filamentous phages, the CTX RS2-encoded gene products mediating replication, integration and repression appear to be novel.

The probability of metastatic disease to the brain from primary NSCLC is correlated with size of the primary tumor, cell type, and intrathoracic lymph node stage.