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Biomedical subjects

X S Wu

Publications and source records attributed to X S Wu.

7 recordsLinked to original sources

In vivo relation of intramyocardial blood volume to myocardial perfusion. Evidence supporting microvascular site for autoregulation.

BACKGROUND: The goal of this study was to explore the role of several factors that affect intramyocardial blood volume by using minimally invasive computed tomography. Anesthetized dogs were scanned with the dynamic spatial reconstructor, a high-speed tomographic scanner, during injection of a bolus of iohexol into the aortic root. METHODS AND RESULTS: In control dogs, it is indicated that the fraction of myocardium that is blood (FMB, %) relates to myocardial perfusion (F, milliliters per gram per minute) in that region as FMB congruent to a.F1/2, where a = 9.5 +/- 1.2% (milliliters times minute per gram)1/2 (mean +/- SD) in the subendocardium and a = 9.6 +/- 1.1% in the subepicardium. In another group of dogs, for the myocardium perfused by a stenosed epicardial artery, a increased to approximately 10 for a 25-43% stenosis (or pressure gradient of 9 mm Hg across narrowing) and to greater than 11 for a 50-55% stenosis (or pressure gradient of 40 mm Hg across narrowing). In these dogs, flow was not impaired under control hemodynamic conditions, but the usual increase of flow (i.e., flow reserve) observed under maximum vasodilation conditions was impaired. In another group of dogs, progressive embolization (using 15-microns-diameter microspheres) of the left ventricular myocardial microcirculation caused the value of a to remain at approximately 9.5 with embolization up to 50% of the fatal dose of microspheres, but it then decreased progressively with embolization to 4.6 at the fatal dose. CONCLUSIONS: We conclude that the FMB/F relation reflects hemodynamic conductance at the microvascular level.

Animals

Genetic analysis of the DNA recognition sequence of the P2 Cox protein.

The Cox protein of temperate Escherichia coli phage P2 is involved in three important biological processes: (i) excision of the integrated prophage genome (G. Lindahl and M. Sunshine, Virology 49:180-187, 1972), (ii) transcriptional repression of the P2 Pc promoter, which controls the expression of the immunity repressor C and the integrase (S. Saha, E. Haggård-Ljungquist, and K. Nordström, EMBO J. 6:3191-3199, 1987), and (iii) transcriptional activation of the late PII promoter of the unrelated satellite phage P4 (S. Saha, E. Haggård-Ljungquist, and K. Nordström, Proc. Natl. Acad. Sci. USA 86:3973-3977, 1989). A comparison of the DNA regions protected by Cox from DNaseI degradation has revealed a presumptive Cox recognition sequence (Saha et al., Proc. Natl. Acad. Sci. USA). The binding region of Cox in the P2 Pc promoter contains three presumptive recognition sequences, "Cox boxes," located in tandem. P2 vir3 and P2 vir24 are virulent deletion mutants unable to plate on Cox-producing strains, most likely because the deletions locate the new early promoters too close to the Cox-binding region (Saha et al., EMBO J.). In this report, spontaneous P2 vir3 and vir24 mutants, no longer sensitive to repression by the Cox protein, have been isolated. These mutants plate with equal efficiency on strains with or without a Cox-producing plasmid, and they have been named cor for cox resistance. Three types are recognized; the four P2 vir3 cor mutants have a 1-base deletion in the first Cox box, while the P2 vir24 cor mutants were of two types; four have a base substitution in the first Cox box, and one has a base substitution in the second Cox box. The effect of the Cox protein on the mutated P2 vir3 and vir24 promoters was analyzed in vivo by using fusions to a promoterless cat (chloramphenicol acetyltransferase) gene. The activities of the P2 vir3 and vir24 early promoters, as opposed to the wild-type early Pe promoter, are drastically reduced by the Cox protein, and the cor mutation renders them as resistant to Cox as the wild-type Pe promoter. Thus, at least the first two Cox boxes are essential for binding of the Cox protein.

Amino Acid Sequence

Efficiency of I-factors in offspring of isogenic lines of Drosophila melanogaster.

In order to obtain information about mechanisms to control the strength of I-effects in Drosophila melanogaster, a genome from a spontaneously arising I-type line was introduced into an isogenic R-type w-K line with cytoplasm of strong R-reactivity. From the homozygous w-K offspring, five families, each with four sublines, were established by single pair-mating for five generations and then mass-mating. In a similar way, another 24 sub-lines were derived from six selected sublines in F9. The strength of the I-effect for the various sublines and sub-sublines was tested at the 8th, 17th, and 18th generations. The results indicated that there was great disparity between and within some families and the trends of family difference remained in successive generations. Such a result supports the hypothesis that the position effect is the main determinant of the I-effect.

Animals

Variation in the strength of R-reactivity and I-inductivity in inbred lines of Drosophila melanogaster.

Two sets of two sister lines of Drosophila melanogaster, with common genome and cytoplasms of different origin, originally showed intermediate R-effects. All four lines had been kept at constant protocol for about 150 generations. From each of the four lines three sublines were established from single females and the strength of R-reactivity was tested by chromosomal loss technique. In two of the four sets, there was heterogeneity between the sublines. One subline in both cases was similar to the three sublines from the sister lines. The remaining two sets remained unchanged. Specific reactions were found in particular combinations of R- and I-lines. Six sets of independently arising I-lines with K-genome showed different response in the strength of their I-inductivity. The evolutionary relation in the strength of R-reactivity of R-type lines and the implication of the specific reactions are discussed.

Animals