LAND USE AND CLIMATE VARIABILITY AMPLIFY CARBON, NUTRIENT, AND CONTAMINANT PULSES: A REVIEW WITH MANAGEMENT IMPLICATIONS

Nonpoint source pollution from agriculture and urbanization is increasing globally at the same time climate extremes have increased in frequency and intensity. We review \u3e200 studies of hydrologic and gaseous fluxes and show how the interaction between land use and climate variability alters magnitude and frequency of carbon, nutrient, and greenhouse gas pulses in watersheds. Agricultural and urban watersheds respond similarly to climate variability due to headwater alteration and loss of ecosystem services to buffer runoff and temperature changes. Organic carbon concentrations/exports increase and organic carbon quality changes with runoff. Nitrogen and phosphorus exports increase during floods (sometimes by an order of magnitude) and decrease during droughts. Relationships between annual runoff and nitrogen and phosphorus exports differ across land use. CH4 and N2O pulses in riparian zones/floodplains predominantly increase with: flooding, warming, low oxygen, nutrient enrichment, and organic carbon. CH4, N2O, and CO2 pulses in streams/rivers increase due to similar factors but effects of floods are less known compared to base flow/droughts. Emerging questions include: (1) What factors influence lag times of contaminant pulses in response to extreme events? (2) What drives resistance/resilience to hydrologic and gaseous pulses? We conclude with eight recommendations for managing watershed pulses in response to interactive effects of land use and climate change

Dysregulated serum IL-23 and SIRT1 activity in peripheral blood mononuclear cells of patients with rheumatoid arthritis.

Sirtuin 1 (Sirt1) is a class III histone deacetylase (HDAC) that modulates gene expression and is involved in the regulation of proinflammatory cytokines. Interleukin-23 (IL-23) is produced by activated macrophages and dendritic cells and could fuel the progression of rheumatoid arthritis (RA). The goal of our study was to evaluate serum IL-23 levels and both Sirt1 activity and expression in peripheral blood mononuclear cells (PBMCs) in patients with RA compared to healthy controls (HC) and to determine the relationship between Sirt1 activity/expression and IL-23 levels. We assessed apoptosis in PBMCs of RA patients and its association with Sirt1 expression and serum IL-23. Serum IL-23 levels were increased in RA patients in comparison with controls. We found a positive correlation between the levels of serum IL-23 and serum IL-6 in RA patients. Decreased cytoplasmic Sirt1 activity was observed in RA patients with severe disease compared to HC. The expression of Sirt1 protein was significantly decreased in PBMCs of RA patients compared to HC using western blotting. Serum IL-23 levels correlated positively with the cytoplasmic Sirt1 activity in RA patients. Apoptosis rate of PBMCs isolated from RA patients was increased compared to HC and correlated negatively with the expression of Sirt1 protein and serum IL-23 levels. Levels of serum IL-23 and Sirt1 activity and expression were disturbed in RA parallel to increased PBMC apoptosis. Our findings might provide the rationale for the development of new therapeutic approaches in RA

Expression of Sirt1 protein is reduced in PBMCs of RA patients compared to HC.

<p>A. Sirt1 protein expression was measured in PBMCs isolated from RA and HC using western blotting as described in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0119981#sec002" target="_blank">Materials and Methods</a>. Beta-actin was used as a loading control. B. Histogram represents Sirt1/beta-actin ratio in PBMCs of healthy controls and patients with RA. Protein levels of Sirt1 and beta-actin were quantified by densitometry using ImageJ 1.40 software. Results were expressed as means ± SD. P = 0.03</p

Biological data of the studied patients with rheumatoid arthritis and healthy controls.

<p>Abbreviations: AFU, Arbitrary fluorescence units; CRP, C-Reactive Protein; ESR, Erythrocyte sedimentation rate; IL, interleukin; TNF, Tumor necrosis factor; na, not available.</p><p>*P value <0.05: significant</p><p>Biological data of the studied patients with rheumatoid arthritis and healthy controls.</p

Serum IL-23 levels correlated negatively with spontaneous apoptosis of PBMCs isolated from RA patients.

<p>A. B. Spontaneous apoptosis of PBMCs from healthy controls and patients with RA after culture in RPMI without serum for 48 hours. Apoptosis was measured by annexin-V assay as reported in the <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0119981#sec002" target="_blank">Materials and Methods</a> chapter. Flow cytometric data are representative of five independent experiments. Percentage of apoptotic cells is indicated. SSC, size scattered count. The histogram summarizes the spontaneous apoptosis of PBMCs from healthy controls and patients with RA after culture in RPMI without serum for 48 hours. The results represent means ± SD. P<0.001. C. Expression of Sirt1 protein correlated negatively with the rate of spontaneous apoptosis in PBMCs isolated from RA patients (r = -0.65). D. Serum levels of IL-23 correlated negatively with apoptosis of PBMCs isolated from RA patients (r = -0.92).</p

Quantification of levels of IL-23, IL-6, IL-8 and TNF in serum of HC and RA subjects.

<p>A. Levels of IL-23, IL-6, IL-8 and TNF in serum of healthy controls and patients with RA. B. Serum levels of IL-23 in subpopulations of RA patients based on DAS 28 score. IL-23, IL-6, IL-8 and TNF were measured by ELISA. Results were expressed as means ± SD. (HC: healthy controls; RA: rheumatoid arthritis).</p

IL-23 levels correlated positively with IL-6 levels in serum of RA patients.

<p>Levels of IL-23 and IL-6 were measured in the serum of RA patients. IL-23 levels correlated positively with IL-6 levels in serum of RA patients (r = 0.62).</p

Prevalence of Self-Reported Venous Thromboembolism and Cardiovascular Risk Factors in Patients with Ulcerative Colitis: The GETAID FOCUS Study

International audienceBackground and aims: Patients with inflammatory bowel disease have an increased risk of venous thromboembolism (VTE) and cardiovascular disease (CVD). The study aims to determine the prevalence of CVD and VTE risk factors in a large population of patients with ulcerative colitis (UC).Methods: We conducted a cross-sectional study in 33 French and Belgium referral centers. A questionnaire was developed to explore self-reported risk factors for VTE and CVD, based on the latest international guidelines, in consecutive patients with UC.Results: A total of 1071 patients with UC were included. There were 539 women (50.3%), and the median age of patients was 44 years [32; 57]. The median disease duration was 10 years [6; 17]. In the cohort, 36.5% of patients reported no cardiovascular risk factor (CVRF) and 72% had ≤ 1 CVRF. Regarding cardiovascular risk markers (CVRM) 36.9% of patients reported no CVRM and 78% had ≤ 1 CVRM. Of the 1071 patients, 91.3% of patients reported no VTE strong risk factor and 96% had ≤ 1 VTE moderate risk factor.Conclusion: This is the first cohort specifically designed to assess both VTE and CVD risks in patients with UC. More than one third of patients with UC had no CVRF and around three quarters had ≤ 1 CVRF. In addition, more than nine out of ten patients had no VTE strong risk factor and ≤ 1 moderate risk factor. Physicians should be aware of these factors in their patients