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Long-term outcome in repaired tetralogy of Fallot (TOF) is related to chronic pulmonary insufficiency (PI), right ventricular (RV) dilation, and deterioration of RV function. The aim of this study was to characterize clinical differences between restrictive and nonrestrictive RV physiology in young patients with repaired TOF.

Background. Atherosclerotic plaque in the descending thoracic aorta (dAo) is related to altered wall shear stress (WSS) for normal patients. Resection with end‐to‐end anastomosis (RWEA) is the gold standard for coarctation of the aorta (CoA) repair, but may lead to altered WSS indices that contribute to morbidity.

The optimal timing of second-stage palliation after Norwood operations remains undefined. Advantages of early cavopulmonary anastomosis are early elimination of volume load and shortening the high-risk interstage period. Potential disadvantages include severe cyanosis, prolonged pleural drainage and hospitalization, and excess mortality. We reviewed our recent experience to evaluate the safety of early cavopulmonary anastomosis.

A major genetic region specifying portions of the carbohydrate structure of Rhizobium leguminosarum CFN42 lipopolysaccharide was analyzed by Tn5 mutagenesis, constructing deletions in cloned DNA, restriction mapping, and complementation analysis. Mutations affecting lipopolysaccharide synthesis were arranged in nine complementation groups spanning 18 kb of DNA. One mutation resulted in O-polysaccharide-containing lipopolysaccharide having a slightly increased mobility in gel electrophoresis. This mutation did not affect the symbiosis with bean plants. The other mutations eliminated the 0-polysaccharide-containing lipopolysaccharide and resulted in strains defective in eliciting bean nodule development.

Previously described Rhizobium leguminosarum bv. phaseoli mutants elicit nodules on bean without infection thread formation. These mutants were shown to be purine or, in one case, pyrimidine auxotrophs. Each of the seven purine auxotrophs grew normally when supplied the penultimate precursor of inosine, 5-aminoimidazole-4-carboxamide riboside. Four seemed blocked early in the purine pathway, because they were also thiamine auxotrophs. Reversion analysis and genetic complementation using cloned wild-type DNA showed that in each mutant a single mutation was responsible for both the symbiotic defect and purine or pyrimidine auxotrophy. The mutations were mapped to five dispersed chromosomal locations. The previously reported weak Calcofluor staining of these mutants on minimal agar appeared to be caused by partial growth on contaminating nutrients in the agar, rather than deficient exopolysaccharide production. Nodulation by the mutants was not enhanced by supplying purine or pyrimidine compounds exogenously. Furthermore, with or without added purine, the purine auxotrophs grew in the root environment as well as the wild type. However, nodulation by the purine auxotrophs was enhanced greatly in the presence of 5-aminoimidazole-4-carboxamide riboside. The results suggest that undiminished metabolic flow through de novo purine biosynthesis, or a particular intermediate in the pathway, is essential in early symbiotic interactions.