Thus, in 8 years non-native Phragmites sequestered

Thus, in 8 years non-native Phragmites sequestered PS-341 in vivo roughly half a year’s worth of the Platte River’s DSi load, beyond what native willow would have done. This result indicates a significant increase in ASi sequestered in sediments – and corresponding decrease in Si flowing downstream – as compared to bare sediments or the more recent native willow sediments that contain far less ASi. Will ASi deposition and sediment fining wrought by Phragmites in the Platte River be stable through time, and eventually become part of the geologic record? There is, of course, no way

of knowing what will happen to these particular deposits. However, the proxies of invasion studied here – biogenic silica and particle size – are widely used in geology to identify various kinds of environmental or ecological change (see, PI3K inhibitor for example, Conley, 1988, Maldonado

et al., 1999 and Ragueneau et al., 1996). Therefore, if conditions are right for preserving and lithifying these sediments, then these signatures of invasion would persist. This study highlights the fact that geomorphologists, geochemists, and ecologists have a lot to learn from each other as they work together to investigate the tremendous scope of environmental change promulgated by human activities. In the example presented here, physical transport of particles is not independent of chemistry, because some particles (like ASi) are bioreactive and may even be produced by plants within the river system. Similarly, elemental fluxes through rivers or other reservoirs are often unwittingly changed by physical alterations of systems. We encourage others to design studies that highlight: (i) physical changes to river systems, like damming or flow reduction from agricultural diversions and evaporative loss, leading to biological

change; and (ii) biological changes in river systems, for example introductions of invasive species, that alter sediment and elemental fluxes to estuaries and coastal oceans. Results from the Platte River demonstrate that non-native Phragmites both transforms dissolved silica into particulate silica and physically sequesters those particles at a much higher rate than filipin native vegetation and unvegetated sites in the same river. Future work will be aimed at disentangling the biochemical and physical components, so that our conceptual framework can be applied to other river systems with different types of vegetation. In addition, high-resolution LiDAR will be used to measure annual erosion and deposition in order to better estimate system-wide rates of Si storage. Scientists are encouraged to look for similar opportunities to study several aspects of environmental change within a single ‘experiment’ because of the benefits such an open-minded, interdisciplinary approach can have towards assessing anthropogenic change.

The summed PAHs found for soybean oil in this study was very simi

The summed PAHs found for soybean oil in this study was very similar to those determined Raf inhibitor in commercial samples (10.4–112.0 μg/kg) by Camargo et al. (2011b). PAHs profile in both studies is practically the same. In Brazil, there is no legislation regarding levels of PAHs in edible oils. There are only maximum benzo[a]pyrene levels established for smoke flavourings (0.03 μg/kg), olive pomace oil (2.0 μg/kg) and drinkable water (0.7 μg/L) ( Brasil, 2003, Brasil, 2004 and Brasil,

2007). When using the maximum limit established by the European Union for B[a]P or the sum for B[a]A, Chy, B[b]F and B[a]P it is possible to observe two situations: in 2007 only one region provided deodorized oils with values higher than 2.0 or 10 μg/kg, but in 2008 three regions reached this mark, with concentrations varying between twice and three times these limits. Throughout the monitoring performed it was possible to observe that due to the different variables involved in oil production and the difficult of controlling the drying by the industry, it is hardly possible buy NVP-BGJ398 to predict the PAHs levels present. The content of PAHs in the crude soybean oils plays an important role in the contamination of the corresponding refined oils. It was noted that although

the refining process reduces the amount of PAH originally present in the crude oil, this effect can be marginal, enhancing the necessity of a better control of the crude oil contamination. Since vegetable oils have been shown to be the major source of PAHs in the diet, a monitoring program should be developed by the oil refining industries and the use of activated carbon during processing is highly recommended. Financial support from FAPESP (Proc.05/59974-8) are gratefully acknowledged. “
“The food industry requires quick and satisfactory methods to ensure product safety and process control.

An interesting and promising alternative to meet this need is the development of sensors that can be used at any stage of food processing. Some authors have addressed the use and development of sensors and biosensors in the food industry and emphasised their advantages, compared to traditional methods of analysis, being more specific, simple and able to provide quick responses with minimal sample preparation mafosfamide steps (Homola et al., 2002, Mello and Kubota, 2002 and Parker and Tothill, 2009). Materials are being sought that are suitable for the development of sensors and biosensors to be applied in various areas of the food industry. Polydiacetylene (PDA) vesicles have been suggested, because PDA-based materials have different colorimetric characteristics, depending on their environment. Changes in their colour, usually from blue to red, in response to stimuli, such as temperature (Guo, Zhang, Jiang, & Liu, 2007), pH (Cheng et al.

The δC 207 0, 163 1, δCH 72 8/5 3, and δCH3 27 9/1 99 (2JHC 207 0

The δC 207.0, 163.1, δCH 72.8/5.3, and δCH3 27.9/1.99 (2JHC 207.0) was compatible with the structure 14, named Talichlorin A (phaeophytin b-151-hidroxy or 152,153-acetyl, 131-carboxilic acid). The δC 170.3, 163.1, δC 111.1 and δOCH3 GSK126 order 53.3/3.57 (3JHC 170.3) were used to propose structure 15 31,32-didehydro-151-hydroxyrhodochlorin-15-acetic acid δ-lactone-152-methyl-173-phytyl ester compared with the literature ( Gandul-Rojas, Gallardo-Guerrero, & Minguez-Mosquera,

1999). The structure of 16 was defined with the δC 170.1, 163.1, δC 111.3 and δOCH3 53.1/3.57 (3JHC 170.3) of the groups used to complete the molecular formula that corresponded to the phaeophytin b peroxylactone or hydroperoxy-Ficuschlorin d. The values of λmax: 430 nm and the EC+ at 429 nm (ψobs + 3.0 mdeg), detected in the UV and CD spectra, respectively, are in accordance with

the effect of 7-formyl, which enhanced the delocalisation of π-electrons, as cited by Lin et al. (2011). The relative stereochemistry of C-181/C-171/C-151 of 13, 15 and 16, and C-181/C-171 of 14, were proposed by the NOESY spectra analyses, and by carbon-13 chemical shift values. The positive signal of Cotton effect was used to attribute Natural Product Library ic50 the same configuration proposed to 12 (132R, 17R, 18R), and 17 (17R, 18R) ( Fig. 2). Seventeen compounds were identified in the stem and leaves of T. triangulare, including four new compounds: one acrylamide and three pheophytins. The quiroptical data of pheophytins are presented for the first time. These detailed analyses do not confirm the presence of some classes of metabolites as proposed by Swarna and Ravindhran (2013) in an extract of T. triangulare. On the other hand, this study showed that the stem and leaves of T. triangulare are rich in nitrogenated compounds that are certainly responsible for the biological properties of this plant. The CD spectra analysis can be used to identify these kinds of phaeophytins in fractions from the plants extracts.

The authors are grateful to Fundação Carlos Chagas de Apoio a Pesquisa do Estado do Rio de Janeiro (FAPERJ), Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES), and to Conselho Nacional de Desenvolvimento Cientifico e Tecnológico Protirelin (CNPq) for scholarships and financial support. “
“Natural trans-fatty acids (TFA) are produced by bio hydrogenation in the rumen of ruminants and occur naturally in ruminant meat (beef, lamb, goat) and dairy products at up to about 5% of total fatty acids (FA) ( Lindmark-Månsson et al., 2003 and Nuernberg et al., 2005). During industrial hydrogenation of oils, TFA are produced from cis-unsaturated fatty acids during heating and in the presence of hydrogen and metal catalysts. Partially hydrogenated oils (containing TFA) were introduced in the food industry due to their longer shelf-life, oxidative stability and semi-solidity at room temperature ( Mozaffarian, Katan, Ascherio, Stampfer, & Willett, 2006).

, 2000) For chemicals with short half-lives, however, the interv

, 2000). For chemicals with short half-lives, however, the interval between the relevant exposure and disease development is often difficult to assess. Study design – along with exposure misclassification discussed later in

this paper – are the most critical and underexplored aspects of biomonitoring studies of short-lived chemicals. Establishing temporality is much more difficult in a “prevalence” study compared to an “incidence” study, which makes it challenging to draw conclusions about causal associations. A typical prevalence study relies on cross-sectional selleck chemical design, which ascertains the exposure and disease information simultaneously (Rothman and Greenland, 1998). When research is focused on short-lived chemicals, many case–control studies – even if they use incident cases – are difficult to interpret because the biomarker levels reflect recent exposures that typically follow rather than precede disease onset. The notable exception is a study that uses samples collected and stored for future use, as is done in nested case–control or case–cohort studies (Gordis, 2008). In a recent review of the epidemiology literature on phthalate metabolites (Goodman et al., 2014) and their association with obesity, diabetes, and cardiovascular disease, most of the studies were cross-sectional in design. The study results GSK1210151A clinical trial were inconsistent across

outcomes and lack of temporality was identified as a key limiting factor in the Morin Hydrate ability to discern relationships between prior exposures to phthalate metabolites and consequent health outcomes. Tier 1 studies are incidence studies that involve a follow-up time period or a longitudinal analysis of repeated measures and allow the establishment of both the time order and the relevant interval between the exposure and the outcome (Table 1). A Tier 2 study would include incidence studies in which

exposure preceded the outcome, but the specific relevant windows of exposure are not considered. The least informative (Tier 3) studies are those that examine the association between current exposure (e.g., blood level of a chemical) and frequently measured outcomes (e.g. BMI) that are likely associated with chronic rather than acute exposures. (Note that this evaluative criterion is not applicable to studies focused on exposure only, such as those examining temporal or spatial relationships within or across populations.) For many short-lived chemicals, there can be large intra-individual temporal variability; attempting to find associations between one measure of such a chemical with disease is not supportable. Differences in biomonitored levels of short-lived chemicals due to changes in an individual’s diet, health, product use, activity and/or location are expected (Pleil and Sobus, 2013). As noted by Meeker et al.

The interaction of Agent codability with Time bin shows that the

The interaction of Agent codability with Time bin shows that the difference in fixations to the “easy” and “hard” agents increased over time. As in Experiment 1, the interaction of Event codability with Time bin shows that speakers directed their gaze to the subject character more rapidly in “easy” events than “hard” events. Fixations between 1000 and 2200 ms. Speakers began looking away from the agent approximately 1000 ms after picture onset and switched their gaze to the patient approximately 1 s later (around speech

onset). At 1000–1200 ms, speakers were generally less likely to fixate “easy” agents than “hard” agents, and more likely to fixate agents in “easy” events than “hard” events; the two factors interacted this website in the by-participant analysis ( Table 5c). There was no three-way interaction Palbociclib with Time bin, indicating that this difference persisted across the entire time window. As a result, speakers also shifted their gaze to the patient most quickly in “easy” events with “easy” agents. Importantly, the strongest predictor of the timing of the gaze shift from agents to patients was Event codability: speakers looked to the patient earlier in “easier” events than “harder” events (an interaction of Event codability with Time bin). Consistent with hierarchical incrementality, this result suggests that speakers were able to begin adding the second character to the sentence earlier in items where

the event gist was easier to encode. Fixations between 0 and 400 ms. Fig. 4c and d shows the timecourse of formulation for items with “easier” and “harder” agents across Prime conditions. Again, speakers were more likely to fixate “easy” agents than “harder” agents across the entire time window: the effect

of Agent codability was reliable in the 0–200 ms time bin (main effect of Agent codability in Table 6a) and was somewhat larger in the 200–400 ms time bin (an interaction of Agent codability with Time was observed in the by-item analysis). As predicted by hierarchical incrementality, early fixations to the agent were influenced by structural priming. Speakers directed fewer fixations to the agent after active primes than after other primes at 0–200 ms (neutral and passive primes; the first contrast for Prime condition in Table 6a); there was no interaction with Time bin, indicating that this difference persisted into the 200–400 ms time bin. The distribution of agent-directed fixations did not differ after neutral and passive primes (the second contrast for Prime condition). The priming effect also did not vary systematically with properties of the agent (no interaction with Agent codability). Fixations between 400 and 1000 ms. Having shifted their attention away from “easy” agents by 400 ms, speakers were less likely to fixate “easy” agents than “hard” agents at 400–600 ms (a main effect of Agent codability; Table 6b).

(2011) based on organic carbon content (Corg) (Eq (3)): equation

(2011) based on organic carbon content (Corg) (Eq. (3)): equation(3) BD=β0+β1·CorgBD=β0+β1·Corg A detailed stem analysis was performed using software that was written specifically for our study in the R programming language (R Development Core Team, 2013). The software enabled the past growth history of a tree stem to be reconstructed. We used the correction proposed by

Carmean (1972) to estimate the height growth of each analysed tree. This method assumes that the annual height growth within a given stem section is constant and that crosscuts occurred in the middle of a given annual height growth. The height increments were calculated for the last 100 years. This time period was selected because of the long period of suppressed growth during

which Selisistat ic50 the trees had not reached a dominant canopy position. The specific basal area increment (SBAI) of a subject tree was chosen as a measure of tree growth rather than the relative growth rate (RGR). Originally, “specific increment” was defined for volume growth ( Bevilacqua, 2002), but we applied this concept to basal area growth. SBAI seems to be a more suitable measure for tree growth because growth is expressed per unit cambial length and does not Angiogenesis inhibitor consider the non-productive inner circle part ( Bevilacqua, 2002 and MacKinnon and MacLean, 2004). The SBAI for the last 5 years was calculated as: equation(4) SBAI5=BA0-BA-5CIRC-5where SBAI5 is the specific basal area increment of the last 5 years, BA0 is the current basal area of a tree, BA−5 is the basal area of a tree before the 5 years and CIRC−5 is the circumference of a section at breast height before the 5 years and represents the length of the cambium (Eq. (4)). As a measure of the competitive influence of neighbouring trees on a subject tree, we calculated the distance-dependent Hegyi competition index (Hegyi, 1974): equation(5) CIi=∑j=1nDj/DiDISTijwhere CIi is the competition index for subject tree i, Dj is the DBH of the jth competitor, Di is the DBH of the subject tree i, DISTij is the distance between the subject tree i and the jth competitor and n is the total number of competitors (Eq. (5)). All species were pooled before calculating the Hegyi competition

index. To determine an optimum search radius (maximum DISTij) and an optimum search DBH (minimum DBHj) above which a tree was considered as a competitor, an optimisation procedure described by Astemizole Miina and Pukkala, 2000 and Vanclay, 2006 was used. We iteratively revised the relative search radius (DISTij) and relative optimum search DBH (DBHj) until we reached a stable optimum (maximum) coefficient of determination adj. R2 between the Hegyi competition index and the SBAI. Multiple linear regressions were used to relate silver fir growth to corresponding soil attributes at single tree level, e.g. soil depth (minimum, mean and maximum value), mean thickness of soil horizons (A, Bw, Bt and E), share of the soil with different profile development (Fig.

6) In Fig 6 (E-SAL), epithelial and endothelial cells were not

6). In Fig. 6 (E-SAL), epithelial and endothelial cells were not present. BMDMC attenuated all these ultrastructural changes and yielded multinucleated cells and type II pneumocytes with large hyperplasia of lamellar bodies. Additionally, epithelial and endothelial cells were noted around the interstitium. Cell therapy also mitigated airway damage, reducing basement membrane irregularity and fragmentation, as well as disorganization and detachment of the airway epithelial cell layer (Table

3, Fig. 6). Y chromosome DNA was not detected in lung tissue at 5 weeks in cell-treated groups. TGF-β, PDGF, and IGF mRNA expressions in lung tissue were higher, while VEGF expression was lower in E-SAL compared to C-SAL. BMDMC administration led to an increase in IGF and VEGF mRNA expressions, and a reduction in TGF-β and PDGF expressions KRX-0401 nmr Selleck Cilengitide (Fig. 7). In the present murine model of pulmonary elatase-induced emphysema, early intravenous BMDMC therapy led to: (1) reduction in mean linear intercept, fraction area of alveolar collapse and hyperinflation; (2) reduction in

the number of mononuclear cells and neutrophils and collagen fiber deposition in lung tissue; (3) increase in elastic fibers in the alveolar septa; (4) decrease in airway epithelium and alveolar-capillary membrane damage as well as elastic fiber breakdown; (5) reduction in the degree of lung apoptotic cells and caspase-3 expression, and (6) improvement of right ventricular wall thickness and right ventricular Amrubicin area followed by a reduction in collagen fibers in lung arterial vessels. Our findings suggest that the lung and heart may be protected by a mechanism linked to a balance between growth factors. In the present study, emphysema was induced by multiple intratracheal instillations of porcine pancreatic elastase. This model, initially described in NMRI

mice (Luthje et al., 2009), leads to lung, cardiovascular, and systemic impairment (Antunes and Rocco, 2011), and induced lung and cardiovascular damage in our C57BL/6 mice. Moreover, this method of emphysema induction yields lengthy progressive inflammatory and remodeling processes, in addition to alveolar destruction. The present study is the first to demonstrate the protective effects of early BMDMC administration to the lung and heart in experimental pulmonary elastase-induced emphysema. To identify this homing of bone marrow cells to the lung parenchyma, we used PCR of Y chromosome-specific sequences. However, Y chromosome DNA was not detected in lung tissue at day 28 in cell-treated groups, suggesting that the benefits we observed probably result from paracrine effects.

3 μM for BIT225, NN-DNJ and Rimantadine, respectively, compared t

3 μM for BIT225, NN-DNJ and Rimantadine, respectively, compared to IC90 values of 30, 30 and 1 μM for SA13/JFH (data not shown). The higher IC90 values reported here compared to previous studies most likely

reflect differences in the duration of treatment, with earlier studies treating infected cells for up to 72 h before measuring extracellular virus infectivity. Since GDC-0068 nmr NN-DNJ can affect glycosylation of viral proteins we limited the duration of treatment to minimise such off-target effects. The efficacy of the inhibitors to limit HCV cell-to-cell transmission was tested using a recently developed single-cycle co-culture assay (Meredith et al., 2013). Since p7 has been reported to play a role in viral internalisation (Griffin et al., 2008) it is important to discriminate the effect of p7 inhibitors on virus assembly and entry. This assay allows one to assess the effect of p7 inhibitor treatment on infected ‘producer’ cells and enables the quantification of new infection events within 2 h of culturing infected and naïve hepatoma cells, which is essential given the reversible nature of p7 targeted compounds click here (Pavlovic et al., 2005 and Pavlovic et al., 2003). HCV J6/JFH or SA13/JFH infected Huh-7.5 cells were treated with 30 μM of either BIT225 or NN-DNJ and 3 μM Rimantadine for 24 h, concentrations previously shown to inhibit the level of infectious extracellular virus by 80–90%. The cells were washed to remove the compounds, labelled

with 5-Chloromethylfluorescein diacetate (CMFDA Cell Tracker Green, Invitrogen), and cultured with naïve Huh-7.5 targets at a 1:1 ratio as detailed in Fig. 1A. We confirmed that all compounds reduced the level of extracellular infectious virus in the co-culture ( Fig. 1B and C), consistent

with a reduction in J6/JFH and SA13/JFH cell-free transmission events. Although all three compounds inhibited 50–70% of J6/JFH cell-to-cell transmission, they had no detectable effect on SA13/JFH cell-to-cell transmission ( Fig. 1C). To determine how wide ranging this effect was, we screened a panel of diverse chimeric viruses expressing the structural proteins from genotype 1–7 for their sensitivity to all currently available p7 inhibitors, including NN-DGJ that does not affect host cell glycosylation pathways ( Chapel et al., 2006a, Chapel et al., 2006b and Chapel et al., 2006c). Depsipeptide cell line Three viruses (JFH-1 – GT2; ED43/JFH – GT3 and QC69/JFH – GT7) showed limited transmission and were excluded from the analysis. The results show that all of the p7 inhibitors were significantly more effective at inhibiting cell-free infection than cell-to-cell transmission when all genotypes are considered ( Fig. 1D). The recent study by OuYang et al., suggest that amantadine binds the p7 ion-channel and locks it into a closed position (OuYang et al., 2013), preventing the de-acidification of the intravesicular compartments and leading to the secretion of non-infectious virus.

07 (N = 22,694, SD = 50 62) In comparison, after winning six tim

07 (N = 22,694, SD = 50.62). In comparison, after winning six times in a row, the figure for mean odds was 0.85 (N = 18,252, SD = 9.82). From the odds that they selected, we can infer that gamblers believed in the gamblers’ fallacy but not in the hot hand. The gambling

results were affected by the gamblers’ choice of odds. One point of odds increase reduced the probability of winning by 0.035 (SD = 0.003, t(36) = 13.403, p < .001). Among all GBP gamblers, the median stake was £14 (N = 371,306, Interquartile Rang = 4.80–53.29). After winning once, the median Gemcitabine in vivo stake went up to £18.47 (N = 178,947, Interquartile Range = 5.04–66.00). After winning twice in a row, the median stake rose to £20.45 (N = 88,036, Interquartile Range = 8.00–80.00) ( Fig. 4, top panel). For the losing side, the opposite was found. People who had lost on more consecutive occasions decreased stakes. After losing once, the median stake went down to £10.89 (N = 192,359, Interquartile Range = 4.00–44.16).

In comparison, after losing twice in a row, the median stake dropped to £10.00 (N = 101,595, Interquartile Range = 3.33–30.00). These trends continued ( Fig. 4, top panel). Gamblers increased stake size after winning and decreased stake size after losing. This could be the result of more money available after winning and less money available after losing. We examined EUR and USD bets. Findings for selected selleck chemical odds were similar (Fig. 3) but those for stake size were less robust (Fig. 4), perhaps because of the reduced sample size. We found evidence for the hot hand but not for the gamblers’ fallacy. Gamblers were more likely to win after winning

and to lose after losing. After winning, gamblers selected safer odds. After losing, they selected riskier odds. Cyclic nucleotide phosphodiesterase After winning or losing, they expected the trend to reverse: they believed the gamblers’ fallacy. However, by believing in the gamblers’ fallacy, people created their own luck. The result is ironic: Winners worried their good luck was not going to continue, so they selected safer odds. By doing so, they became more likely to win. The losers expected the luck to turn, so they took riskier odds. However, this made them even more likely to lose. The gamblers’ fallacy created the hot hand. Ayton and Fischer (2004) found that people believed in the gamblers’ fallacy for natural events over which they had no control. Our gamblers displayed the gamblers’ fallacy for actions (i.e. bets) that they took themselves. This may indicate that they did not believe that bets were under their control. Fong, Law, and Lam (2013) reported Chinese gamblers believed their luck would continue. Does this mean they felt they had more control over their bets? By believing their luck would continue, did they help to bring it to an end? There are likely to be other domains (e.g., financial trading) where people reduce their preference for risk in the wake of chance success and thereby give the impression of a hot hand.

Chlorophyll extract was measured as fluorescence and converted to

Chlorophyll extract was measured as fluorescence and converted to concentration using spinach extract standards. Rock surface area was determined by water volume displacement ( Cooper and Testa, 2001) and epilithic algal biomass reported as μg Chl a cm−2 rock. Leaf material

was processed within a few days of collection to determine mass loss and fungal colonization from each stream site. Leaves were removed from each bag and gently rinsed with deionized water to remove sandy debris. From each leaf bag, ergosterol content (as an indication of fungal biomass) and organic leaf decay rates were determined. Ergosterol concentration (μg Ergosterol mg−1 ash-free dry weight (AFDW) leaf) was measured from 30 haphazardly collected hole punches of leaf tissue. Ergosterol was extracted from leaf punches by incubating in methanol for 2 h followed see more by potassium hydroxide hydrolysis at 80 °C (Newell et al., 1988). Next, sterols were isolated through a pentane extraction at 21 °C. Pentane soluble sterol extracts were dried under a constant stream of N2 gas and re-dissolved in methanol for high pressure liquid chromatography (HPLC) analysis. The separation module (Waters 2695) injected 100 μl of solution through the column (Novapak C18) at a rate of 1.5 ml min−1. The Waters 2998 detector was set

at an absorbance of 282λ. Retention times and concentrations were compared to a pure ergosterol standard (Fluka HPLC grade > 95%; Newell et al., 1988). For leaf loss rates, leaves were dried in an oven at 60 °C until constant weight was reached. Leaf weights were corrected for the 30

Z-VAD-FMK order hole punches taken for ergosterol. Dry leaves were ground and a subsample taken to determine AFDW (i.e., leaf organic content) by ashing in a muffle oven for 5 h at 550 °C. Sugar maple leaf decay rates (k) were calculated for each point using the negative natural log of the percent AFDW remaining at the end of the incubation ( Petersen and Cummins, 1974). Dissolved O2 and N2 concentrations from leaf incubations were determined using membrane inlet mass spectrometry (MIMS) from N2:Ar and O2:Ar ratios (Kana et al., 1994). Ar ratios were converted to concentrations using gas saturated water standards at 20 and 30 °C Protein tyrosine phosphatase and by applying Henry’s law with published gas constants for Ar, N2, and O2 (Lide and Frederikse, 1995 and Wilhelm et al., 1977). O2 and N2 flux rates were calculated as the difference between initial and final gas concentrations divided by the incubation time. Leaf biofilm oxygen consumption (e.g., O2 uptake; R) and denitrification rates (e.g., N2 flux) were expressed as μg gas h−1 g−1 AFDW leaf. Prior to analysis, parameters were grouped as follows: (1) landscape, (2) water quality, (3) DOM characteristics, and (4) benthic. One N2 flux measurement was removed as an outlier prior to analysis because this point had a z-score < −4 (i.e., greater than 4 standard deviations way from the mean) and poor analytical reproducibility on multiple sample injections.