Black carbon affects the cycling of non-black carbon in soil

Black carbon (BC) is an important fraction of many soils worldwide and plays an important role in global C biogeochemistry. However, few studies have examined how it influences the mineralization of added organic matter (AOM) and its incorporation into soil physical fractions and whether BC decomposition is increased by AOM. BC-rich Anthrosols and BC-poor adjacent soils from the Central Amazon (Brazil) were incubated for 532 days either with or without addition of (13)C-isotopically different plant residue. Total C mineralization from the BC-rich Anthrosols with AOM was 25.5% (P < 0.05) lower than with mineralization from the BC-poor adjacent soils. The AOM contributed to a significantly (P < 0.05) higher proportion to the total C mineralized in the BC-rich Anthrosols (91-92%) than the BC-poor adjacent soils (69-80%). The AOM was incorporated more rapidly in BC-rich than BC-poor soils from the separated free light fraction through the intra-aggregate light fraction into the stable organo-mineral fraction and up to 340% more AOM was found in the organo-mineral fraction. This more rapid stabilization was observed despite a significantly (P < 0.05) lower metabolic quotient for BC-rich Anthrosols. The microbial biomass (MB) was up to 125% greater (P < 0.05) in BC-rich Anthrosols than BC-poor adjacent soils. To account for increased MB adsorption onto BC during fumigation extraction, a correction factor was developed via addition of a (13)C-enriched microbial culture. The recovery was found to be 21-41 % lower (P < 0.05) for BC-rich than BC-poor soils due to re-adsorption of MB onto BC. Mineralization of native soil C was enhanced to a significantly greater degree in BC-poor adjacent soils compared to BC-rich Anthrosols as a result of AOM. No positive priming by way of cometabolism due to AOM could be found for aged BC in the soils. (C) 2009 Elsevier Ltd. All rights reserved.

Kinin-B2 Receptor Activity Determines the Differentiation Fate of Neural Stem Cells

Bradykinin is not only important for inflammation and blood pressure regulation, but also involved in neuromodulation and neuroprotection. Here we describe novel functions for bradykinin and the kinin-B2 receptor (B2BkR) in differentiation of neural stem cells. In the presence of the B2BkR antagonist HOE-140 during rat neurosphere differentiation, neuron-specific beta 3-tubulin and enolase expression was reduced together with an increase in glial protein expression, indicating that bradykinin- induced receptor activity contributes to neurogenesis. In agreement, HOE-140 affected in the same way expression levels of neural markers during neural differentiation of murine P19 and human iPS cells. Kinin-B1 receptor agonists and antagonists did not affect expression levels of neural markers, suggesting that bradykinin-mediated effects are exclusively mediated via B2BkR. Neurogenesis was augmented by bradykinin in the middle and late stages of the differentiation process. Chronic treatment with HOE-140 diminished eNOS and nNOS as well as M1-M4 muscarinic receptor expression and also affected purinergic receptor expression and activity. Neurogenesis, gliogenesis, and neural migration were altered during differentiation of neurospheres isolated from B2BkR knock-out mice. Whole mount in situ hybridization revealed the presence of B2BkR mRNA throughout the nervous system in mouse embryos, and less beta 3-tubulin and more glial proteins were expressed in developing and adult B2BkR knock-out mice brains. As a underlying transcriptional mechanism for neural fate determination, HOE-140 induced up-regulation of Notch1 and Stat3 gene expression. Because pharmacological treatments did not affect cell viability and proliferation, we conclude that bradykinin-induced signaling provides a switch for neural fate determination and specification of neurotransmitter receptor expression.

Interactions between the NO-Citrulline Cycle and Brain-derived Neurotrophic Factor in Differentiation of Neural Stem Cells

The diffusible messenger NO plays multiple roles in neuroprotection, neurodegeneration, and brain plasticity. Argininosuccinate synthase (AS) is a ubiquitous enzyme in mammals and the key enzyme of the NO-citrulline cycle, because it provides the substrate L-arginine for subsequent NO synthesis by inducible, endothelial, and neuronal NO synthase (NOS). Here, we provide evidence for the participation of AS and of the NO-citrulline cycle in the progress of differentiation of neural stem cells (NSC) into neurons, astrocytes, and oligodendrocytes. AS expression and activity and neuronal NOS expression, as well as L-arginine and NOx production, increased along neural differentiation, whereas endothelial NOS expression was augmented in conditions of chronic NOS inhibition during differentiation, indicating that this NOS isoform is amenable to modulation by extracellular cues. AS and NOS inhibition caused a delay in the progress of neural differentiation, as suggested by the decreased percentage of terminally differentiated cells. On the other hand, BDNF reversed the delay of neural differentiation of NSC caused by inhibition of NOx production. Alikely cause is the lack of NO, which up-regulated p75 neurotrophin receptor expression, a receptor required for BDNF-induced differentiation of NSC. We conclude that the NO-citrulline cycle acts together with BDNF for maintaining the progress of neural differentiation.

BK virus associated meningoencephalitis in an AIDS patient treated with HAART

A severely immune-suppressed AIDS patient was suspected of suffering from BK virus (BKV) meningoencephalitis, after being studied for common causes of neurological complications of co-infectious origin. Polymerase chain reaction (PCR) and sequence analysis of cerebrospinal fluid and brain samples, confirmed the presence of BKV. His clinical condition improved along with the regression of brain lesions, after modifications on his antiretroviral regime. Five months after discharge, the patient was readmitted because of frequent headaches, and a marked inflammatory reaction was evidenced by a new magnetic resonance imaging (MRI). The symptoms paralleled a rising CD4+ lymphocyte count, and immune reconstitution syndrome was suspected. This is the first non-postmortem report of BKV meningoencephalitis in an AIDS patient, showing clinical and radiographic improvement solely under HAART.