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In this study, our goal was to adapt the moss layer transfer technique (MLTT), first developed to restore degraded Sphagnum‐dominated peatland explicitly with a bryophyte layer, to a former in‐situ oil sands well‐pad constructed with nearby mineral fill in northwestern Alberta, Canada. Mineral fill was either completely removed or partially removed with residual fill buried under excavated and decompacted peat, followed by the transfer of donor moss collected from nearby linear features with different plant communities in peatlands. Three years after MLTT, peatland vegetation covers 63% of the site. Carex spp. dominate with 36% coverage, followed by mosses at 12%, including 3% Sphagnum spp. and 8% fen mosses, and shrubs at 8%. Different substrate adjustment treatments and types of donor moss had negligible impact on vegetation development although areas without MLTT remained devoid of mosses and had the lowest peatland species cover. Instead, surface elevation, moisture conditions, and substrate chemistry played important roles in shaping the vegetation communities. The prompt introduction and establishment of peatland donor species through MLTT was crucial to the overall re‐establishment of peatland vegetation. This is the first full pad scale study to prove that a flat, moist peat surface created by the removal and/or burial of mineral fill can support peatland vegetation development, particularly ground layer bryophytes. Overall, the reclaimed well‐pad appears to be on trajectory toward becoming a functional peatland and our approaches should be considered and tested in future well‐pad reclamation trials. [ABSTRACT FROM AUTHOR]

Across Canada's boreal forest, disturbances from in situ oil sands mining, including well‐pads, significantly impact vast areas of the landscape. The creation of well‐pads requires removal of vegetation and placement of mineral fill, which essentially stops any carbon (C) sequestration on the once peatland ecosystem. It is important that, once no longer in use, these well‐pads are restored as long‐term C (peat) accumulation is what defines peatland ecosystem. However, little is known about the recovery of greenhouse gas exchange post‐restoration of these features. We studied a decommissioned well‐pad located in a treed poor fen that was restored using three soil adjustment treatments (SATs): (1) complete mineral fill removal (Peat‐Dec); (2) partial pad removal and burial under peat layer (BUPL); and (3) mixing mineral and peat by inversion (Mixed‐P‐M). The recreated peat surface was revegetated with donor peatland species using the moss layer transfer technique (MLTT). The objectives of this paper were to (1) quantify plot‐scale seasonal carbon dioxide (CO2) and methane (CH4) exchange of the SATs, 2–4 years post‐restoration compared to reference sites and (2) determine the influence of several environmental variables on CO2 and CH4 exchange. All SATs proved effective in recreating a soil surface needed to support peatland vegetation as shown by similar rates of net ecosystem exchange (NEE). Equally, both types of vegetation reintroduced led this site on a trajectory toward functioning as a net C sink. [ABSTRACT FROM AUTHOR]

Across Canada's boreal forest, linear disturbances, including cutlines such as seismic lines and roads, crisscross the landscape to facilitate resource exploration and extraction; many of these linear disturbances cross peatland ecosystems. Changes in tree canopy cover and the compression of the peat by heavy equipment alter local thermal, hydrological, and ecological conditions, likely changing carbon exchange on the disturbance, and possibly in the adjacent peatland. We measured bulk density, water table, soil temperature, plant cover, and CO2 and CH4 flux along triplicate transects crossing a winter road through a wooded fen near Peace River, Alberta, Canada. Sample plots were located 1, 5, and 10 m from the road on both sides with an additional three plots on the road. Productivity of the overstory trees, when present, was also determined. The winter road had higher bulk density, shallower water table, higher graminoid cover, and thawed earlier than the adjacent peatland. Tree productivity and CO2 flux varied between the plots, and there was no clear pattern in relation to distance from the road. The plots on the winter road acted as a greater CO2 sink and greater CH4 source compared to the adjacent peatland with plots on the winter road emitting on average (standard error) 479 (138) compared to 41 (10) mg CH4 m−2 day−1 in the adjacent peatland. Considering both gases, global warming potential increased from 70 to 250 g CO2e m−2 year−1 in the undisturbed area to 2100 g CO2e m−2 year−1 on the winter road. Although carbon fluxes on any given cutline through peatland will vary depending on level of compaction, line width and vegetation community shifts, the large number of linear disturbances in Canada's boreal forest and slow recovery on peatland ecosites suggest they could represent an important anthropogenic greenhouse gas source. [ABSTRACT FROM AUTHOR]

Background Ethanol ( Et OH) exposure prior to traumatic injury, such as a burn, elevates systemic and local inflammatory responses and increases morbidity and mortality. Adipose is a large tissue mass that is often inflamed during obesity or other stresses, which disturbs metabolic homeostasis. To date, there has been little investigation into the inflammatory response of adipose tissue after combined Et OH exposure and burn injury. Methods Two Et OH exposure regimens were utilized to examine the role of inflammation in adipose tissue after Et OH and burn injury. Mice were either given a single or episodic binge exposure to Et OH or saline followed by scald (burn) or sham injury 30 minutes later. Twenty-four hours post injury, serum and adipose tissue were collected for assessment of inflammatory mediators. Results Single binge Et OH alone induced no inflammation in adipose when compared with sham vehicle-treated mice. However, single binge Et OH followed by burn injury induced significant elevations in m RNA and protein concentrations of pro-inflammatory mediators interleukin-6 ( IL-6), KC, and monocyte chemoattractant protein 1 compared with either insult alone or sham vehicle group. Additionally, Et OH exposure and burn injury significantly blunted inducible nitric oxide synthase (i NOS), indicating a complex inflammatory response. Episodic binge Et OH exposure followed by burn injury exacerbated the postburn adipose inflammatory response. The magnitude of the episodic binge-induced inflammatory parameters postburn were 2- to 5-fold greater than the response detected after a single exposure of Et OH, indicating Et OH-induced potentiation of burn-induced inflammatory response. Finally, inflammatory loci and crown-like structures in adipose were significantly increased by episodic binge Et OH and burn injury. Conclusions This is the first report of binge and burn-induced crown-like structure formation. Evidence presented herein suggests an important role for alcohol and burn as an additional mediator of adipose inflammation in postburn injury, a common complication in burn patients. [ABSTRACT FROM AUTHOR]

Background: Clinical and laboratory evidence suggests that alcohol consumption prior to burn injury leads to dysregulated immune function and subsequent higher rates of morbidity and mortality. Our laboratory previously observed higher levels of pro-inflammatory cytokines and leukocyte infiltration in the lungs of mice following ethanol and burn injury. To understand the mechanism of the increased inflammatory response, we looked at different signaling initiators of inflammation including toll-like receptors 2 and 4 (TLR2 and 4) pathways. Methods: Wild-type, TLR2, and TLR4 knockout mice were treated with vehicle or a single binge dose of ethanol (1.11 g/kg) and subsequently given a sham or burn injury. Twenty-four hours postinjury, systemic and pulmonary levels of pro-inflammatory cytokines were quantified, and differences in neutrophil infiltration were determined by histological examination. Results: Higher numbers of neutrophils were observed in the lungs of wild-type mice following the combined insult of ethanol and burn injury relative to either injury alone. This increase in leukocyte accumulation was absent in the TLR4 knockout mice. Circulating levels of IL-6 and tumor necrosis factor-α were also elevated in wild-type mice but not in TLR4 knockout mice. Consistent with these findings, pulmonary levels of KC and IL-6 were increased in wild-type mice following burn and ethanol compared to burn injury alone as well as to their TLR4 knockout counterparts. In contrast, TLR2 knockout mice displayed similar levels, to wild-type mice, of neutrophil infiltration as well as IL-6 and KC in the lung. Conclusions: These data suggest that TLR4 signaling is a crucial contributory component in the exuberant inflammation after ethanol and burn injury. However, TLR2 does not appear to play a vital role in the aberrant pulmonary inflammation. [ABSTRACT FROM AUTHOR]