Flux of dimethylsulfide (DMS) from ocean surface waters is the predominant natural source of sulfur to the atmosphere and influences climate by aerosol formation. Marine bacterioplankton regulate sulfur flux by converting the precursor dimethylsulfoniopropionate (DMSP) either to DMS or to sulfur compounds that are not climatically active. Through the discovery of a glycine cleavage T-family protein with DMSP methyltransferase activity, marine bacterioplankton in the Roseobacter and SAR11 taxa were identified as primary mediators of DMSP demethylation to methylmercaptopropionate. One-third of surface ocean bacteria harbor a DMSP demethylase homolog and thereby route a substantial fraction of global marine primary production away from DMS formation and into the marine microbial food web.

We used wounded Drosophila embryos to define an evolutionarily conserved pathway for repairing the epidermal surface barrier. This pathway includes a wound response enhancer from the Ddc gene that requires grainy head (grh) function and binding sites for the Grh transcription factor. At the signaling level, tyrosine kinase and extracellular signal-regulated kinase (ERK) activities are induced in epidermal cells near wounds, and activated ERK is required for a robust wound response. The conservation of this Grh-dependent pathway suggests that the repair of insect cuticle and mammal skin is controlled by an ancient, shared control system for constructing and healing the animal body surface barrier.

[1] As part of the Large-Scale Biosphere-Atmosphere Experiment in Amazonia (LBA), PM 10 aerosol was collected during both the wet and dry (biomass burning) seasons of 1999 and analyzed for total water-soluble organic nitrogen (WSON), urea, and 17 amino acids. In addition to total WSON the inorganic N species nitrate (NO 3 À ), nitrite (NO 2 À ), and ammonium (NH 4 + ) were also analyzed. WSON was found to represent $45% (mean concentration $3.5 nmol N/m 3 ) and $43% (mean concentration $61 nmol N/m 3 ) of the total N in wet and dry season aerosol samples, respectively. Urea and amino N made up $19% of the total organic N in dry season aerosols and $2.5% of the total organic N in wet season aerosols; the majority of WSON, $80% in the dry season and $97% in the wet season, remained uncharacterized. The results suggest that biomass burning is a source of WSON, yet poorly understood (since this data set represents the first study of WSON in the context of biomass burning). Future studies aimed at determining the magnitude of WSON released from biomass burning globally, its species composition, and its biogeochemical significance are needed.

SUMMARYAcute inflammation in response to injury is a tightly regulated process by which subsets of leukocytes are recruited to the injured tissue and undergo behavioural changes that are essential for effective tissue repair and regeneration. The diabetic wound environment is characterised by excessive and prolonged inflammation that is linked to poor progression of healing and, in humans, the development of diabetic foot ulcers. However, the underlying mechanisms contributing to excessive inflammation remain poorly understood. Here we show in a murine model that the diabetic environment induces stable intrinsic changes in haematopoietic cells. These changes lead to a hyper-responsive phenotype to both pro-inflammatory and anti-inflammatory stimuli, producing extreme M1 and M2 polarised cells. During early wound healing, myeloid cells in diabetic mice show hyperpolarisation towards both M1 and M2 phenotypes, whereas, at late stages of healing, when non-diabetic macrophages have transitioned to an M2 phenotype, diabetic wound macrophages continue to display an M1 phenotype. Intriguingly, we show that this population predominantly consists of Gr-1+ CD11b+ CD14+ cells that have been previously reported as ‘inflammatory macrophages’ recruited to injured tissue in the early stages of wound healing. Finally, we show that this phenomenon is directly relevant to human diabetic ulcers, for which M2 polarisation predicts healing outcome. Thus, treatments focused at targeting this inflammatory cell subset could prove beneficial for pathological tissue repair.

Impaired wound healing in diabetic patients is associated with deficiencies in the production of factors involved in cell proliferation and migration, such as vascular endothelial growth factor. However, it remains unclear how the transcriptional regulation of the genes encoding these factors is affected by the diabetic environment. Hypoxia-inducible factor-1alpha (Hif-1alpha), the regulatory subunit of the Hif-1 transcription factor, plays an important role in activating many of these genes. Therefore, we tested whether Hif-1alpha function is impaired in the diabetic wound environment and whether restoring Hif-1 function improves wound healing. Here, we show that Hif-1alpha protein levels are dramatically reduced in wounds of leptin receptor-deficient diabetic mice compared with nondiabetic littermates. Reduction in Hif-1alpha levels results in decreased DNA-binding activity and in decreased expression of several Hif-1 target genes, including vascular endothelial growth factor, heme oxygenase-1, and inducible nitric oxide synthase. Furthermore, we demonstrate that sustained expression of Hif-1alpha in leptin receptor-deficient diabetic wounds restores expression of these factors, enhances angiogenesis, and significantly accelerates wound healing. Taken together, these results suggest that Hif-1alpha function plays a significant role in wound healing and reduced levels of Hif-1alpha may contribute to impaired healing.

During the Southern Hemispheric spring of 2000 (during the months of November and early December), rain, bulk and size‐separated aerosol samples were collected at the Cape Grim Baseline Air Pollution Station located on the island of Tasmania, Australia and analyzed for total organic nitrogen (N), urea, and dissolved free amino acids. Rain and bulk aerosol samples contained organic N at concentrations representing, on average, between 19 and 25% of total N. Urea was not detected in the six rain samples analyzed. However, urea represented ∼24% of the organic N contained in nonbaseline aerosol samples, and ∼2% of the organic N contained within baseline samples. Trajectory analysis combined with meteorological data indicated that high concentrations of urea within aerosols were mainly due to Tasmanian sources, likely animal emissions, although the application of urea fertilizers cannot be dismissed as a source. In nonbaseline samples the highest concentrations of urea were associated with the coarse mode aerosol (>1 μm), although urea was also found in the fine mode aerosol (<1 μm), potentially indicating gas‐to‐particle conversion of urea. Aerosol samples collected in marine air masses contained urea within an intermediate fraction centered at ∼1 μm suggesting the sea surface microlayer as a source. Dissolved free amino acids contributed ∼53% of the organic N in rain, but were not a significant proportion of the total organic N fraction in either nonbaseline or baseline aerosol samples. Due to their presence in rain, amino acids likely exist in aerosols as unhydrolyzed proteins. In cascade impactor samples highly influenced by marine sources, profiles for amino N were inversely related to urea N, possibly indicating live species and the sea surface microlayer as a source for organic N.

Wound repair requires both the recruitment and coordination of numerous cell types including inflammatory cells, fibroblasts, endothelial and epithelial cells. Each cell type has a distinct set of cell behavior such as formation of granulation tissue and basement membrane, migration, proliferation and redifferentiation. These processes are dependent on cell-cell and cell-ECM signaling, intracellular signal transduction cascades, and ultimately, changes in gene transcription. We have investigated the role of the transcription factor HOXA3 in wound repair and angiogenesis. Here we show that HOXA3 increases endothelial cell migration, induces angiogenesis in vivo, and leads to increased expression of the matrix metalloproteinase-14 (MMP-14) and urokinase-type plasminogen activator receptor (uPAR) genes in endothelial cells in culture and in vivo in response to injury. We find that HOXA3 gene expression is upregulated during wound healing in angiogenic endothelial cells and keratinocytes, and that HOXA3 is not induced in genetically diabetic mice that have impaired angiogenesis and wound repair. We demonstrate that gene transfer of HOXA3 into diabetic mouse wounds leads to dramatic improvements in both angiogenesis and wound closure. In addition, we show that HOXA3 promotes migration of endothelial cells and keratinocytes in a uPAR-dependent manner. Together these findings illustrate how the morphoregulatory protein, HOXA3 can facilitate tissue remodeling via coordinated changes in both epithelial and endothelial cell gene expression and behavior in adult tissues during wound repair.

From March through early May of 2000, rain and bulk aerosol samples were collected at a coastal site on the eastern Mediterranean Sea at Erdemli, Turkey, and analyzed for nitrogen (N) species, including nitrate (NO3−), nitrite (NO2−), ammonium (NH4+), water‐soluble organic N, urea, and dissolved free amino acids. Other ions were also analyzed, including Ca2+, Mg2+, K+, Na+, Cl−, and SO42−. Water‐soluble organic N was found to contribute ∼17% and ∼26% of the total water‐soluble N in rain and aerosols, respectively. Organic N concentrations within rain and aerosols exhibited statistically significant linear relationships to Ca2+ ion (Rsqr ∼ 0.75, P < 0.05), suggesting a relationship to calcite (CaCO3) in atmospheric dust. Kinematic trajectory analyses indicated the origin of winds from arid regions, mainly in northern Africa, in 70% of the aerosols sampled. Earth Probe/Total Ozone Mapping Spectrometer aerosol index data also confirmed the influence of atmospheric dust in the region on days when Ca2+ concentrations were elevated, and trajectory analyses suggested northern Africa as a source region. The combined ion, trajectory, and aerosol index data suggest that organic N is associated with atmospheric dust in this region. Urea N and amino N represented a small percentage of the organic N fraction. In rain and aerosols, urea represented ∼11% and <1%, respectively, of the total organic N. While amino N contributed minimally to organic N totals (∼1% of total organic N in aerosols), the individual amino acids contributing ∼75% of amino N were indicative of biological organisms. Further research is needed to decipher the influence from biology and gas phase adsorption of anthropogenically derived water‐soluble organics on organic N totals.