Fractionation of sulfur and oxygen isotopes in sulfate by soil sorption.

Both field and laboratory data indicate that there is no significant isotope fractionation of sulfate during sorption in upland forest Podzols. The dominant sulfate sorption process in these soils is adsorption onto mineral surfaces. In the Plastic Lake watershed, Dorset, Ontario, Canada, fractions of sulfate from Podzol B-horizons have the following mean isotope (%.) compositions: water soluble sulfate, δ34S = +6.4; δ18O = -5.3; bicarbonate-exchanged sulfate by two methods,δ34S = + 4.5 and + 3.4; δ18O =-6.2 and -5.6; dissolved sulfate in B-horizon soilwater seepage,δ34S = + 4.8; δ18O = -5.4. These data indicate that soil sorption enriches dissolved sulfate in 34S by approximately 1 ± 1%. and in 18O by 0 +- 1 %. relative to sorbed sulfate. Similar results were obtained by laboratory sorption of sulfate by prepared goethite, which is a mineral representative of soil sorption sites in acidic Podzols like the one at Plastic Lake. The mean fractionation between sorbed and dissolved sulfate was found to be - 0.3%. for34S and 0.1 %. for 18O. Earlier literature has confused the term adsorption; in many cases the more general term sorption, or retention, should be used. Pronounced fractionation of S and O isotopes in sulfate by lake and ocean sediments has been attributed to "adsorption" or "retention" but is more likely the result of sulfate reduction. Apparently, at Earth-surface conditions the only substantial isotope shifts in sulfate occur during microbial processes

Sulfate dynamics in upland forest soils, central and southern Ontario, Canada: Stable isotope evidence.

In a Podzol (central Ontario) and a Brunisol-Luvisol (southern Ontario), SO4 in soil seepage is buffered by various mechanisms including microbial cycling and sorption-desorption. A large portion of the water-soluble SO4 in these soils is not derived from soil water, but is apparently desorbed from soil matrix. A HCO3-exchange procedure extracts even more sorbed SO4, especially from the acidic Podzol B horizon. The SO4 in these soils has a range in δ34S values similar to that of atmospheric SO4 input. In contrast, the δ18O (avg. + 4 to + 8.5) values of the soil SO4 are depleted by 2-9% relative to atmospheric SO4 input (δ18O = + 11 to + 13) due to rapid biological cycling of soil S. This cycling includes biological assimilation of SO4 and production of secondary SO4, which is depleted in 18O. Calculations based on δ18O data of litter leaching experiments indicate that approximately 50-100% of seepage SO4 in the LFH and B horizons at Plastic Lake, central Ontario, is secondary. Biological cycling apparently exerts an important control on net release or retention of S by oils. Seasonal variations in soil water evaporation and litterfall may be important factors affecting the δ18O of soil SO4, and may be partly responsible for the 10% seasonal shift in δ18O of LFH horizon SO4

Ovotestes and XY sex reversal in a female with an interstitial 9q33.3-q34.1 deletion encompassing NR5A1 and LMX1B causing features of Genitopatellar syndrome.

Contains fulltext : 51503.pdf (publisher's version ) (Closed access)We describe our findings in a 46,XY female with a clinical features of Genitopatellar syndrome (GPS) and confirmed hermaphroditism with ovotestes, and five additional patients with GPS. GPS is a genetic disorder characterized by renal and genital anomalies, joint dislocation, aplastic or hypoplastic and often displaced patellae, minor facial anomalies, and mental retardation. The genital anomalies clearly distinguish GPS from nail-patella syndrome (NPS) that has similar features, but additionally shows hypoplastic finger- and toenails as found in the 46,XY female. In our patients no mutation was found in the coding regions of WNT4, WNT7A, TBX4, and LMX1B. Fluorescent in situ hybridization (FISH) and array-based comparative genome hybridization (aCGH) analysis showed a 3 Mb deletion of LMX1B, NR6A1, and NR5A1 (SF1) in the 46,XY female. This is the first report of a microdeletion causing haploinsuffiency of LMX1B and NR5A1. The deletion of LMX1B is responsible for the knee anomalies and the deletion of NR5A1 likely causes the sex reversal. Cytogenetic analysis of the five additional patients with diagnosed GPS failed to identify a similar microdeletion, or inversion of a potentially regulatory element between the two genes. This suggests that the locus 9q33-9q34 can be excluded for GPS and that the presented case is unique in its combination of GPS and NPS features caused by a microdeletion associated with loss of function of LMX1B and NR5A1