This review highlighted the fact that few studies examined the use of simulation in nursing education through learning theories and via assessment of core competencies. It also identified observational tools used to assess competencies in action, as holistic and context-dependent constructs.

These conflicting results called into question the validity of localization of a QTL by linkage followed by the use of a congenic strain made with an incomplete chromosome coverage. To resolve this issue, we constructed five new congenic strains, designated C17S.L1 to C17S.L5, that completely spanned the Ϯ2 LOD confidence interval supposedly containing the QTL. Each congenic strain was made by replacing a segment of the DSS rat by that of the normotensive Lewis (LEW) rat. The only section to be LL homozygous is the region on Chr 17 specified in a congenic strain, as evidenced by a total genome scan. The results showed that BPs of C17S.L1 and C17S.L2 were lower (P Ͻ 0.04) than that of DSS rats. In contrast, BPs of C17S.L3, C17S.L4, and C17S.L5 were not different (P Ͼ 0.6) from that of DSS rats. Consequently, a BP QTL must be located in an interval of ϳ15 cM shared between C17S.L1 and C17S.L2 and unique to them both, as opposed to C17S.L3, C17S.L4, and C17S.L5. The present study illustrates the importance of thorough chromosome coverage, the necessity for a genome-wide screening, and the use of "negative" controls in physically mapping a QTL by congenic strains.Dahl salt-sensitive rat; normotensive Lewis rat; congenic strain; congenic substrain THE PRESENCE OF A BLOOD PRESSURE (BP) quantitative trait locus (QTL) on rat chromosome 17 (Chr 17) was originally hinted on by linkage analyses of an F2 population derived from a cross between the Dahl salt-sensitive (DSS) and Lewis (LEW) rats (6). The maximum LOD score supporting this localization was 2.9, which constitutes a suggestive linkage (6). Subsequently, another group of investigators using a different model of salt-sensitive hypertension, the Sabra strain, independently localized a QTL by linkage to a similar region, but with a higher LOD score of 3.43 (27). Employing recombinant inbred strains derived from crosses between the spontaneously hypertensive (SHR) and Brown Norway (BN) rats (22), a separate group of investigators did not find linkage to BP, but they found linkage to the left ventricular mass in a region on Chr 17 distant from the interval containing the BP QTL reported in DSS and Sabra rats (6, 27). Recently, researchers studying cardiac hypertrophy associated with pulmonary hypertension (28) showed that a QTL for right ventricular mass was localized to a Chr 17 region close to the BP QTL in DSS (6) and Sabra (27) strains. Finally, linkage analysis based on the Lyon rats also showed that a QTL on Chr 17 was involved in controlling metabolic homeostasis and BP (3).Nevertheless, the BP QTL localization (6) was questioned because a congenic strain made by replacing a segment of the DSS chromosome with that of LEW did not show any BP effect (12). Due to a lack of markers at the time, the entire Ϯ2 LOD support interval harboring the QTL was not replaced in that study (12). Consequently, the validity of the QTL could not be verified.For the convenience of presentation and discussion, the congenic strain previously made (12) is designated as congenic 1. Beca...

Pursuing fully a suggestion from linkage analysis that there might be a quantitative trait locus (QTL) for blood pressure (BP) in a chromosome (Chr) 2 region of the Dahl salt-sensitive rat (DSS), four congenic strains were made by replacing various fragments of DSS Chr 2 with those of Lewis (LEW). Consequently, a BP QTL was localized to a segment of around 3 cM or near 3 Mb on Chr 2 by comparative congenics. The BP-augmenting alleles of this QTL originated from the LEW rat, a normotensive strain compared with DSS. The dissection of a QTL with such a paradoxical effect illustrated the power of congenics in unearthing a gene hidden in the context of the whole animal system, presumably by interactions with other genes. The locus for the angiotensin II receptor AT-1B (Agtr1b) is not supported as a candidate gene for the QTL because a congenic strain harboring it did not have an effect on BP. There are approximately 19 known and unknown genes present in the QTL interval. Among them, no standout candidate genes are reputed to affect BP. Thus the QTL will likely represent a novel gene for BP regulation.

Elongation factor Tu (EF-Tu), encoded by tuf genes, carries aminoacyl-tRNA to the ribosome during protein synthesis. Duplicated tuf genes (tufA and tufB), which are commonly found in enterobacterial species, usually coevolve via gene conversion and are very similar to one another. However, sequence analysis of tuf genes in our laboratory has revealed highly divergent copies in 72 strains spanning the genus Yersinia (representing 12 Yersinia species). The levels of intragenomic divergence between tufA and tufB sequences ranged from 8.3 to 16.2% for the genus Yersinia, which is significantly greater than the 0.0 to 3.6% divergence observed for other enterobacterial genera. We further explored tuf gene evolution in Yersinia and other Enterobacteriaceae by performing directed sequencing and phylogenetic analyses. Phylogenetic trees constructed using concatenated tufA and tufB sequences revealed a monophyletic genus Yersinia in the family Enterobacteriaceae. Moreover, Yersinia strains form clades within the genus that mostly correlate with their phenotypic and genetic classifications. These genetic analyses revealed an unusual divergence between Yersinia tufA and tufB sequences, a feature unique among sequenced Enterobacteriaceae and indicative of a genus-wide loss of gene conversion. Furthermore, they provided valuable phylogenetic information for possible reclassification and identification of Yersinia species.