The Effect of Biological Soil Crusts on Throughput of Rainwater and N into Lake Michigan Sand Dune Soils

Biological soil crusts composed of cyanobacteria, green algae, bryophytes, and lichens colonize soils in arid and semiarid ecosystems worldwide and are responsible for significant N input to the soils of these ecosystems. Soil crusts also colonize active sand dunes in more humid regions, but studies of structure and function of such sand dune crusts are lacking. We identified the cyanobacterial, algal, and bryophytic constituents and N production and leachates of biological soil crusts that colonize beach dunes at the Indiana Dunes National Lakeshore along southern Lake Michigan in Indiana, USA. To determine the role of these crusts in this system, we conducted a greenhouse experiment in which intact soil cores with biological crusts were subjected to artificial rainfall over a full growing season. The volume and N content of leachate from the cores were quantified in relation to degree of crust development, taxonomic composition, rainfall volume and intensity, light intensity, and the presence of plant litter. Net N throughput significantly exceeded N inputs to cores in rainwater. Net N outputs from crusts to subsurface soil ranged from 0. 01 to 0.19 g NH ₄ ⁺ -N m⁻² yr⁻¹ and 0.01 to 0.61 g NO ₃ ^– N m⁻² yr⁻¹. Thus, total inorganic N inputs associated with biological soil crusts ranged from 0.02 g N m⁻² yr⁻¹ to 0.8 g N m⁻² yr⁻¹. High volume (≥2 cm) rainfall resulted in more N leaching than low volume events, and plant litter added over the surface of crusted soil cores significantly increased the amount of N in leachate. Exploratory path analysis revealed direct and indirect linkages among environmental factors, crust development, and crust composition in regulating the throughput of H₂O and N from these intact soil cores. Biological soil crusts at this site, combined with other properties of the soil surface, substantially increase N inputs to this water- and nutrient-limited sand dune ecosystem.     

Listeria monocytogenes Infection Causes Metabolic Shifts in Drosophila melanogaster

Immunity and metabolism are intimately linked; manipulating metabolism, either through diet or genetics, has the power to alter survival during infection. However, despite metabolism''s powerful ability to alter the course of infections, little is known about what being “sick” means metabolically. Here we describe the metabolic changes occurring in a model system when Listeria monocytogenes causes a lethal infection in Drosophila melanogaster. L. monocytogenes infection alters energy metabolism; the flies gradually lose both of their energy stores, triglycerides and glycogen, and show decreases in both intermediate metabolites and enzyme message for the two main energy pathways, beta-oxidation and glycolysis. L. monocytogenes infection also causes enzymatic reduction in the anti-oxidant uric acid, and knocking out the enzyme uric oxidase has a complicated effect on immunity. Free amino acid levels also change during infection, including a drop in tyrosine levels which may be due to robust L. monocytogenes induced melanization.     

ICAMs Are Not Obligatory for Functional Immune Synapses between Naive CD4 T Cells and Lymph Node DCs

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Insulin increases H<Subscript>2</Subscript>O<Subscript>2</Subscript>-induced pancreatic beta cell death

Insulin resistance results, in part, from impaired insulin signaling in insulin target tissues. Consequently, increased levels of insulin are necessary to control plasma glucose levels. The effects of elevated insulin levels on pancreatic beta (β) cell function, however, are unclear. In this study, we investigated the possibility that insulin may influence survival of pancreatic β cells. Studies were conducted on RINm, RINm5F and Min-6 pancreatic β-cells. Cell death was induced by treatment with H₂O₂, and was estimated by measurements of LDH levels, viability assay (Cell-Titer Blue), propidium iodide staining and FACS analysis, and mitochondrial membrane potential (JC-1). In addition, levels of cleaved caspase-3 and caspase activity were determined. Treatment with H₂O₂ increased cell death; this effect was increased by simultaneous treatment of cells with insulin. Insulin treatment alone caused a slight increase in cell death. Inhibition of caspase-3 reduced the effect of insulin to increase H₂O₂-induced cell death. Insulin increased ROS production by pancreatic β cells and increased the effect of H₂O₂. These effects were increased by inhibition of IR signaling, indicative of an effect independent of the IR cascade. We conclude that elevated levels of insulin may act to exacerbate cell death induced by H₂O₂ and, perhaps, other inducers of apoptosis.     

Bipolar‐associated miR‐499‐5p controls neuroplasticity by downregulating the Cav1.2 subunit CACNB2

Bipolar disorder (BD) is a chronic mood disorder characterized by manic and depressive episodes. Dysregulation of neuroplasticity and calcium homeostasis are frequently observed in BD patients, but the underlying molecular mechanisms are largely unknown. Here, we show that miR‐499‐5p regulates dendritogenesis and cognitive function by downregulating the BD risk gene CACNB2. miR‐499‐5p expression is increased in peripheral blood of BD patients, as well as in the hippocampus of rats which underwent juvenile social isolation. In rat hippocampal neurons, miR‐499‐5p impairs dendritogenesis and reduces surface expression and activity of the L‐type calcium channel Cav1.2. We further identified CACNB2, which encodes a regulatory β‐subunit of Cav1.2, as a direct functional target of miR‐499‐5p in neurons. miR‐499‐5p overexpression in the hippocampus in vivo induces short‐term memory impairments selectively in rats haploinsufficient for the Cav1.2 pore forming subunit Cacna1c. In humans, miR‐499‐5p expression is negatively associated with gray matter volumes of the left superior temporal gyrus, a region implicated in auditory and emotional processing. We propose that stress‐induced miR‐499‐5p overexpression contributes to dendritic impairments, deregulated calcium homeostasis, and neurocognitive dysfunction in BD.     

Maintenance of redox state and pancreatic beta-cell function: role of leptin and adiponectin

Whereas oxidative stress is linked to cellular damage, reactive oxygen species (ROS) are also believed to be involved in the propagation of signaling pathways. Studies on the role of ROS in pancreatic beta‐cell physiology, in contrast to pathophysiology, have not yet been reported. In this study we investigate the importance of maintaining cellular redox state on pancreatic beta‐cell function and viability, and the effects of leptin and adiponectin on this balance. Experiments were conducted on RINm and MIN6 pancreatic beta‐cells. Leptin (1–100 ng/ml) and adiponectin (1–100 nM) increased ROS accumulation, as was determined by DCFDA fluorescence. Using specific inhibitors, we found that the increase in ROS levels was mediated by NADPH oxidase (Nox), but not by AMP kinase (AMPK) or phosphatidyl inositol 3 kinase (PI3K). Leptin and adiponectin increased beta‐cell number as detected by the XTT method, but did not affect apoptosis, indicating that the increased cell number results from increased proliferation. The adipokines‐induced increase in viability is ROS dependent as this effect was abolished by N‐acetyl‐L‐cysteine (NAC) or PEG‐catalase. In addition, insulin secretion was found to be regulated by alterations in redox state, but not by adipokines. Finally, the effects of the various treatments on activity and mRNA expression of several antioxidant enzymes were determined. Both leptin and adiponectin reduced mRNA levels of superoxide dismutase (SOD)1. Adiponectin also decreased SOD activity and increased catalase and glutathione peroxidase (GPx) activities in the presence of H₂O₂. The results of this study show that leptin and adiponectin, by inducing a physiological increase in ROS levels, may be positive regulators of beta‐cell mass. J. Cell. Biochem. 113: 1966–1976, 2012. © 2012 Wiley Periodicals, Inc.     

Mitochondrial DNA variation in Indo-Pacific populations of the giant tiger prawn,Penaeus monodon

Surveys of mitochondrial DNA (mtDNA) variation in the giant tiger prawn, Penaeus monodon, using restriction fragment length polymorphisms have provided the first clear evidence that the Indo-West Pacific region is a site of accumulation of genetic diversity rather than a site of origin of genetic diversity. No haplotyes were found in common between a group of five southeast African populations and a group of five Australian (including Western Australia) and three southeast Asian populations. The dominant haplotype was different in the Australian and southeast Asian population groups. Genetic diversity (pi) was greatest in Indonesia (pi averaged 0.05), less in the Philippines and Australia (pi averaged 0.01), and markedly less in the southeast African and the West Australian populations (pi averaged 0.003). The high diversity of the southeast Asian populations resulted from the occurrence in those populations of a set of haplotypes found only in southeast Asia but derived from the southeast African haplotypes. These genetic variants therefore evolved in the Indian Ocean and later migrated into the Indo-West Pacific region. Low genetic variation in the geographically marginal populations in southeast Africa and Western Australia is considered to be the result of bottlenecks, but mismatch distributions suggest that large population sizes have been maintained in Indonesian populations for long periods.     

The Interactions of Porcine and Ovine,Serum and Colostral Immunoglobulins with Staphylococcal Protein A

The purpose of these studies was to determine the proportion of each immunoglobulin class/subclass in blood and colostrum of the pig and sheep, which would bind to staphylococcal Protein A. The concentrations of porcine IgG, IgM, and IgA were determined for serum and colostral whey from five sows. Similar measurements were made on two fractions produced by elution of the sample through a Protein A-Sepharose column: fraction 1, immunoglobulins which did not bind to Protein A, and fraction 2, immunoglobulins which bound to Protein A. The concentrations of ovine IgG₁, IgG₂, IgM, and IgA were measured for serum and colostral whey from six ewes, and again similar measurements were made after elution of each ovine sample through Protein A-Sepharose. All classes/subclasses of porcine and ovine serum and colostral immunoglobulins bound to Protein A to some extent. More than 90% of IgG from both porcine colostral whey and serum bound to Protein A. Ovine IgG₁ from most ewes possessed a low affinity for Protein A whereas ovine IgG₂ generally possessed a high affinity; 100% of the IgG₂ in ovine colostral whey samples bound to Protein A. There was remarkable variation between individuals in the binding capacity of porcine IgM and each of the ovine immunoglobulins. For the ovine samples, in particular there were distinct differences between Protein A binding capacity of serum and colostral immunoglobulins of the same class/subclass.