Design of Managed Aquifer Recharge for Agricultural and Ecological Water Supply Assessed Through Numerical Modeling

The Walla Walla Basin, in Eastern Oregon and Washington, USA, faces challenges in sustaining an agricultural water supply while maintaining sufficient flow in the Walla Walla River for endangered fish populations. Minimum summer river flow of 0.71 m³/s is required, forcing irrigators to substitute groundwater from a declining aquifer for lost surface water diversion. Managed Aquifer Recharge (MAR) was initiated in 2004 attempting to restore groundwater levels and improve agricultural viability. The Integrated Water Flow Model (IWFM) was used to compute surface and shallow groundwater conditions in the basin under water management scenarios with varying water use, MAR, and allowable minimum river flow. A mean increase of 1.5 m of groundwater elevation, or 1.5 % of total aquifer storage, was predicted over the model area when comparing maximum MAR and no MAR scenarios where minimum river flow was increased from current level. When comparing these scenarios a 53 % greater summer flow in springs was predicted with the use of MAR. Results indicate MAR can supplement irrigation supply while stabilizing groundwater levels and increasing summer streamflow. Potential increase in long-term groundwater storage is limited by the high transmissivity of the aquifer material. Increased MAR caused increased groundwater discharge through springs and stream beds, benefiting aquatic habitat rather than building long-term aquifer storage. Judicious siting of recharge basins may be a means of increasing the effectiveness of MAR in the basin.This is an author's peer-reviewed final manuscript, as accepted by the publisher. The published article is copyrighted by Springer and can be found at: http://link.springer.com/journal/11269Keywords: Managed aquifer recharge, Salmon, Hydrological modeling, Groundwater management, Habitat restoration, Agricultural water suppl

Thyroid function tests and characterization of thyroxine-binding globulin in the carbohydrate-deficient glycoprotein syndrome type I.

Carbohydrate-deficient glycoprotein (CDG) syndrome is a newly recognized hereditary disorder that presents with psychomotor retardation, cerebellar ataxia, peripheral sensorimotor neuropathy, and, variably, skeletal abnormalities, lipodystrophy, and retinitis pigmentosa. These abnormalities appear to be produced by a defect that causes reduced carbohydrate content in glycoproteins. We studied seven patients with CDG type I belonging to five unrelated families. The concentration of serum TBG, a glycoprotein of hepatic origin, was measured by RIA and T4 saturation and was found to be below the normal range in three of the seven patients and normal in four of them. More than half of the total serum TBG had reduced sialic acid content and localized on isoelectric focusing (IEF) as two prominent bands cathodal to the three major bands of normal TBG. The latter two bands are responsible for the characteristic IEF pattern or CDG syndrome. TBG in patients with CDG had immunoreactivity indistinguishable from that of normal TBG and had normal affinity for T4, T3, and rT3. Serum total T4, T3, and rT3 were below the normal range in seven, five, and seven patients, respectively. The free T4 index was also below normal in four patients, but the free T4 concentration, measured by equilibrium dialysis at low dilution, and serum TSH were in the midnormal range. The serum total T4 and rT3 levels were disproportionately reduced relative to the serum TBG concentration and compared to the concentrations of these iodothyronines in matched subjects with inherited partial TBG deficiency. Chronic illness cannot explain these changes, because, contrary to patients with nonthyroidal illness, those with CDG had significantly higher serum total T3/T4 and lower rT3/T4 ratios. It is concluded that IEF of TBG is a rapid and simple method for the diagnosis of CDG type I and that the abnormal pattern can be detected as early as 5 days postpartum. Patients with CDG are chemically euthyroid, and it is postulated that the reduction in serum iodothyronine concentrations beyond that explained on the basis of low TBG levels may be due to the interference with binding to TBG by an unidentified substance