MBFR

AcronymDefinition
MBFRMutual & Balanced Force Reduction
MBFRMuscular Blood Flow at Rest (radiology)
References in periodicals archive ?
It suggested that the high concentrations of sulfate have some extent inhabitation to denitrification in MBfR processes.
Performance of MBfR under High Concentration of Sulfate.
It indicated that the nitrate would be utilized preferentially by denitrification bacteria (DB) than sulfate utilized by SRB in completion with [H.sub.2] in MBfR, and nitrate respiration is energetically more favorable than sulfate respiration [31].
In the autohydrogenotrophic denitrification in MBfR, the SRB also utilized hydrogen as electron donor to reduce sulfate to sulfide; therefore, there would be a competition for hydrogen between the reductions of nitrate, sulfate, and other electron acceptors.
The study investigated the performance of MBfR to remove nitrate companied with high influent concentrations of sulfate over 155 days.
Rittmann, "Effect of pH on nitrate and selenate reduction in flue gas desulfurization brine using the [H.sub.2]-based membrane biofilm reactor (MBfR)," Water Science & Technology, vol.
When patients were stratified according to status of CAD diagnosis (known versus suspected), there was a significant inverse correlation between MBFR and HgbA1c% (r = -0.279, P = 0.01) in patients with suspected, but not known CAD.
Using a MBFR cutoff value of >2 as normal, the variables of sex, age, obesity (BMI [greater than or equal to] 30kg/[m.sup.2]), smoking status, dyslipidemia, duration of T2DM, presence of CAD, and/or hypertension were included in the univariate models, and HgbA1c% > 7.1% significantly increased the risk for having abnormal MBFR (unadjusted odds ratio: 1.84, 95% CI: 1.10-3.11, P = 0.02).
We found that patients with poor control of their T2DM, defined as HgbA1c > 7.1%, had poorer myocardial microcirculatory perfusion, as evidenced by lower MBFR values.
In our study, after adjusting for those possible confounders, HgbA1c > 7.0% remained significantly associated with abnormal MBFR (defined as <2).
Our results would support the findings in those studies as well, in that we observed that HgbA1c level had less apparent effect on the MBFR in those with established CAD, suggesting that when the microcirculation has been irreversibly affected by chronic glycemic elevations, there may be no benefit to achievement of tighter glycemic control.
The observed inverse relationship between HgbA1c and MBFR in T2DM patients without known CAD suggests that improved glycemic control may reduce the likelihood of subsequent cardiovascular events.