Longer thaw seasons increase nitrogen availability for leaching during fall in tundra soils

Climate change has resulted in warmer soil temperatures, earlier spring thaw and later fall freeze-up, resulting in warmer soil temperatures and thawing of permafrost in tundra regions. While these changes in temperature metrics tend to lengthen the growing season for plants, light levels, especially in the fall, will continue to limit plant growth and nutrient uptake. We conducted a laboratory experiment using intact soil cores with and without vegetation from a tundra peatland to measure the effects of late freeze and early spring thaw on carbon dioxide (CO2) exchange, methane (CH4) emissions, dissolved organic carbon (DOC) and nitrogen (N) leaching from soils. We compared soil C exchange and N production with a 30 day longer seasonal thaw during a simulated annual cycle from spring thaw through freeze-up and thaw. Across all cores, fall N leaching accounted for ~33% of total annual N loss despite significant increases in microbial biomass during this period. Nitrate $({{{\rm{NO}}}_{3}}^{-})$ leaching was highest during the fall (5.33 ± 1.45 mg N m−2 d−1) following plant senescence and lowest during the summer (0.43 ± 0.22 mg N m−2 d−1). In the late freeze and early thaw treatment, we found 25% higher total annual ecosystem respiration but no significant change in CH4 emissions or DOC loss due to high variability among samples. The late freeze period magnified N leaching and likely was derived from root turnover and microbial mineralization of soil organic matter coupled with little demand from plants or microbes. Large N leaching during the fall will affect N cycling in low-lying areas and streams and may alter terrestrial and aquatic ecosystem nitrogen budgets in the arctic

Association of childhood type 1 diabetes mellitus with a variant of PAX4: possible link to beta cell regenerative capacity

Aims/hypothesis: Loss of pancreatic beta cells is the crucial event in the development of type 1 diabetes. It is the result of an imbalance between autoimmune destruction and insufficient regeneration of islet cells. To study the role of islet cell regeneration in the pathogenesis of type 1 diabetes, we focused on PAX4, a paired homeodomain transcriptional repressor that is involved in islet cell growth. Methods: The study included 379 diabetic children and 1,070 controls from two distinct populations, and a cohort of children who had not developed type 1 diabetes, despite the presence of islet cell antibodies. Genomic DNA analysis of PAX4 was carried out via direct sequencing of PCR-amplified fragments and allelic discrimination. We compared the transrepression potential of the PAX4 variants in βTC3 cells and analysed their influence on beta cell growth. Results: The type 1 diabetic subjects are different from the normal individuals in terms of the genotype distribution of the A1168C single nucleotide polymorphism in PAX4. The C/C genotype is frequent among type 1 diabetic children (73%) and rare among the control population (32%). Conversely, the A/C genotype is prevalent among control subjects (62%) and antibody-positive children without type 1 diabetes (73.6%), but uncommon among subjects with type 1 diabetes (17.5%). The combination of PAX4A and PAX4C is functionally more active than PAX4C alone (the ‘diabetic' variant). Beta cells expressing PAX4A and PAX4C efficiently proliferate when stimulated with glucose, whereas cells expressing the PAX4C variant alone do not. Conclusions/interpretation: We have identified a link between beta cell regenerative capacity and susceptibility to type 1 diabetes. This finding could explain the fact that not all of the individuals who develop autoimmunity against beta cells actually contract the disease. The C/C genotype of the A1168C polymorphism in PAX4 can be viewed as a predisposition marker that can help to detect individuals prone to develop type 1 diabete

Tumor promoter phorbol myristate acetate inhibits Ca2+ influx through voltage-gated Ca2+ channels in two secretory cell lines, PC12 and RINm5F.

Protein kinase C is known to be involved both in initiation and termination of cellular responses due to phosphoinositide breakdown. Here we report that in PC12 cells (a line of neurosecretory cells derived from a rat pheochromocytoma), pretreatment with nanomolar concentrations of phorbol myristate acetate, PMA, which is believed to specifically activate protein kinase C, inhibits the cytosolic-free Ca2+ concentration rise induced by depolarizing agents. In contrast, plasma membrane potential and 45Ca efflux from preloaded cells were unaffected by PMA pretreatment. Inhibition by PMA and diacylglycerol of the cytosolic-free Ca2+ concentration rise induced by depolarization was observed also in another cell line, the insulin secreting line RINm5F. These results raise the possibility that the voltage-gated Ca2+ channel is under inhibitory control by protein kinase C

Suppression of Pdx-1 perturbs proinsulin processing, insulin secretion and GLP-1 signalling in INS-1 cells

Aims/hypothesis: Mutations in genes encoding HNF-4α, HNF-1α and IPF-1/Pdx-1 are associated with, respectively, MODY subtypes-1, -3 and -4. Impaired glucose-stimulated insulin secretion is the common primary defect of these monogenic forms of diabetes. A regulatory circuit between these three transcription factors has also been suggested. We aimed to explore how Pdx-1 regulates beta cell function and gene expression patterns. Methods: We studied two previously established INS-1 stable cell lines permitting inducible expression of, respectively, Pdx-1 and its dominant-negative mutant. We used HPLC for insulin processing, adenovirally encoded aequorin for cytosolic [Ca2+], and transient transfection of human growth hormone or patch-clamp capacitance recordings to monitor exocytosis. Results: Induction of DN-Pdx-1 resulted in defective glucose-stimulated and K+-depolarisation-induced insulin secretion in INS-1 cells, while overexpression of Pdx-1 had no effect. We found that DN-Pdx-1 caused down-regulation of fibroblast growth factor receptor 1 (FGFR1), and consequently prohormone convertases (PC-1/3 and -2). As a result, DN-Pdx-1 severely impaired proinsulin processing. In addition, induction of Pdx-1 suppressed the expression of glucagon-like peptide 1 receptor (GLP-1R), which resulted in marked reduction of both basal and GLP-1 agonist exendin-4-stimulated cellular cAMP levels. Induction of DN-Pdx-1 did not affect glucokinase activity, glycolysis, mitochondrial metabolism or ATP generation. The K+-induced cytosolic [Ca2+] rise and Ca2+-evoked exocytosis (membrane capacitance) were not abrogated. Conclusions/interpretation: The severely impaired proinsulin processing combined with decreased GLP-1R expression and cellular cAMP content, rather than metabolic defects or altered exocytosis, may contribute to the beta cell dysfunction induced by Pdx-1 deficienc

Relationship between river size and nutrient removal

Author Posting. © American Geophysical Union, 2006. This article is posted here by permission of American Geophysical Union for personal use, not for redistribution. The definitive version was published in Geophysical Research Letters 33 (2006): L06410, doi:10.1029/2006GL025845.We present a conceptual approach for evaluating the biological and hydrological controls of nutrient removal in different sized rivers within an entire river network. We emphasize a per unit area biological parameter, the nutrient uptake velocity (νf), which is mathematically independent of river size in benthic dominated systems. Standardization of biological parameters from previous river network models to νf reveals the nature of river size dependant biological activity in these models. We explore how geomorphic, hydraulic, and biological factors control the distribution of nutrient removal in an idealized river network, finding that larger rivers within a basin potentially exert considerable influence over nutrient exports.This work was funded by NASA-IDS (NNG04GH75G), NSF-LTER OCE-9726921, and NOAA (NA17RJ2612- 344 to Princeton U.)

Dynamics of N removal over annual time periods in a suburban river network

Author Posting. © American Geophysical Union, 2008. This article is posted here by permission of American Geophysical Union for personal use, not for redistribution. The definitive version was published in Journal of Geophysical Research 113 (2008): G03038, doi:10.1029/2007JG000660.River systems are dynamic, highly connected water transfer networks that integrate a wide range of physical and biological processes. We used a river network nitrogen (N) removal model with daily temporal resolution to evaluate how elevated N inputs, saturation of the denitrification and total nitrate removal processes, and hydrologic conditions interact to determine the amount, timing and distribution of N removal in the fifth-order river network of a suburban 400 km2 basin. Denitrification parameters were based on results from whole reach 15NO3 tracer additions. The model predicted that between 15 and 33% of dissolved inorganic nitrogen (DIN) inputs were denitrified annually by the river system. Removal approached 100% during low flow periods, even with the relatively low and saturating uptake velocities typical of surface water denitrification. Annual removal percentages were moderate because most N inputs occurred during high flow periods when hydraulic conditions and temperatures are less favorable for removal by channel processes. Nevertheless, the percentage of annual removal occurring during above average flow periods was similar to that during low flow periods. Predicted river network removal proportions are most sensitive to loading rates, spatial heterogeneity of inputs, and the form of the removal process equation during typical base flow conditions. However, comparison with observations indicates that removal by the river network is higher than predicted by the model at moderately high flows, suggesting additional removal processes are important at these times. Further increases in N input to the network will lead to disproportionate increases in N exports due to the limits imposed by process saturation.This work was funded by NSF-DEB- 0614282, NSF-OCE-9726921, NSF-DEB-0111410, and NSF-BCS- 0709685