Determining blood and plasma volumes using bioelectrical response spectroscopy.

We hypothesized that an electric field (inductance) produced by charged blood components passing through the many branches of arteries and veins could assess total blood volume (TBV) or plasma volume (PV). Individual (N = 29) electrical circuits (inductors, two resistors, and a capacitor) were determined from bioelectrical response spectroscopy (BERS) using a Hewlett Packard 4284A Precision LCR Meter. Inductance, capacitance, and resistance from the circuits of 19 subjects modeled TBV (sum of PV and computed red cell volume) and PV (based on 125I-albumin). Each model (N = 10, cross validation group) had good validity based on 1) mean differences (-2.3 to 1.5%) between the methods that were not significant and less than the propagated errors (+/- 5.2% for TBV and PV), 2) high correlations (r > 0.92) with low SEE (< 7.7%) between dilution and BERS assessments, and 3) Bland-Altman pairwise comparisons that indicated "clinical equivalency" between the methods. Given the limitation of this study (10 validity subjects), we concluded that BERS models accurately assessed TBV and PV. Further evaluations of the models' validities are needed before they are used in clinical or research settings.

The regulation of exopolysaccharide production is important at two levels of nodule development in Rhizobium meliloti.

We show that two exopolysaccharide overproducing Tn5 mutants of Rhizobium meliloti, exoR and exoS, have distinct symbiotic defects. While the exoR mutant is unable to colonize nodules, the exoS mutant retains that ability but varies in its ability to produce nitrogen-fixing nodules. We correlate these defects with different degrees of exopolysaccharide overproduction and growth impairment. We further show that the exoR mutant is able to enter developing infection threads but is unable to invade nodule cells. The exoR mutant gives rise to spontaneous pseudorevertants containing second-site suppressor mutations that decrease exopolysaccharide synthesis. These pseudorevertants form nitrogen-fixing nodules. Although the suppressor mutations have the opposite effect on exopolysaccharide production compared to the exoS::Tn5 mutation, they consistently map to the exoS::Tn5 region and belong to the same genetic complementation group as defined by transposon insertion mutations. The effect of the suppressor mutations on exopolysaccharide production is correlated with effects on the expression of exo genes involved in exopolysaccharide synthesis. Finally, we provide evidence that the exoR gene is not required for the regulation of exopolysaccharide synthesis by ammonia.