Global phosphorus retention by river damming

More than 70,000 large dams have been built worldwide. With growing water stress and demand for energy, this number will continue to increase in the foreseeable future. Damming greatly modifies the ecological functioning of river systems. In particular, dam reservoirs sequester nutrient elements and, hence, reduce downstream transfer of nutrients to floodplains, lakes, wetlands, and coastal marine environments. Here, we quantify the global impact of dams on the riverine fluxes and speciation of the limiting nutrient phosphorus (P), using a mechanistic modeling approach that accounts for the in-reservoir biogeochemical transformations of P. According to the model calculations, the mass of total P (TP) trapped in reservoirs nearly doubled between 1970 and 2000, reaching 42 Gmol y⁻¹, or 12% of the global river TP load in 2000. Because of the current surge in dam building, we project that by 2030, about 17% of the global river TP load will be sequestered in reservoir sediments. The largest projected increases in TP and reactive P (RP) retention by damming will take place in Asia and South America, especially in the Yangtze, Mekong, and Amazon drainage basins. Despite the large P retention capacity of reservoirs, the export of RP from watersheds will continue to grow unless additional measures are taken to curb anthropogenic P emissions.The systematic damming of rivers began with the onset of the Industrial Revolution and peaked in the period from 1950 to 1980 (1, 2). After slowing down during the 1990s, the pace of dam building has recently risen again sharply (3). As a consequence, the number of hydroelectric dams with generating capacity >1 MW is expected to nearly double over the next two decades (2). The current surge in dam construction will increase the proportion of rivers that are moderately to severely impacted by flow regulation from about 50% at the end of the 20th century to over 90% by 2030 (3). Homogenization of river flow regimes resulting from damming is a growing, worldwide phenomenon and has been invoked as one of the reasons for the decline in freshwater biodiversity (4).Another major global driver of environmental change of river systems is enrichment by anthropogenic nutrients, in particular phosphorus (P) (5, 6). Fertilizer use, soil erosion, and the discharge of wastewater have more than doubled the global P load to watersheds compared with the inferred natural baseline (7–10). Because P limits or colimits primary productivity of many aquatic ecosystems, increased river fluxes of P have been identified as a main cause of eutrophication of surface water bodies, including lakes and coastal marine environments (6, 11, 12). River damming and P enrichment are interacting anthropogenic forcings, because sediments accumulating in reservoirs trap P and, thus, reduce the downstream transfer of P along the river continuum (13–15). This raises the question to what extent P retention by dams may offset anthropogenic P enrichment of rivers.The number of published studies from which P retention efficiencies in dam reservoirs can be obtained is small: an extensive literature search only yields useable data for 155 reservoirs (Dataset S1), that is, less than 0.2% of the ∼75,000 dam reservoirs larger than 0.1 km² (16). The existing data nonetheless clearly show that even a single dam can significantly alter the flow of P along a river. For example, dam-impounded Lake Kariba (Zambezi River), Lake Diefenbaker (South Saskatchewan River), and Lac d’Orient (Seine River) sequester ∼87%, 94%, and 71% of their total P inflows, respectively (17–19). For the 1 million km² Lake Winnipeg watershed, 28 reservoirs and lakes accumulate over 90% of the total P load (18). The global retention of P by dams, however, remains poorly constrained (20, 21). Previous estimations have simply applied a correction factor to river P loads to represent retention by dams (22–24). This approach does not distinguish between the various chemical forms of P, nor does it account for differences in reservoir hydraulics or provide information about uncertainties on retention estimates.Here, we follow a mass balance modeling approach developed previously to calculate the global retention of nutrient silicon by dams (25). The mass balance model represents the key biogeochemical processes controlling P cycling in reservoirs (Fig. 1). The model separates total P (TP) into the following pools: total dissolved P (TDP); particulate organic P (POP); exchangeable P (EP); and unreactive particulate P (UPP). UPP consists mostly of crystalline phosphate minerals that are inert on reservoir-relevant timescales (≤100 y); TDP comprises inorganic and organic forms of P, whereas EP includes orthophosphate and organic P molecules sorbed to or coprecipitated with oxides, clay minerals, and organic matter. Reactive P (RP) is defined as the sum of TDP, EP, and POP; RP represents the potentially bioavailable fraction of TP.Open in a separate windowFig. 1.Mass balance model used to estimate retention of P in reservoirs. F_in,i is the influx of the ith P pool into the reservoir, F_i,out is the corresponding efflux out of the reservoir, F₁₂ represents P fixation by primary productivity, F₂₁ represents mineralization of POP, F₁₃ and F₃₁ are the sorption and desorption rates of dissolved P, and F_i,bur is the permanent burial flux of the ith particulate P pool in the reservoir’s sediments.Global predictive relationships for the retention of TP and RP in reservoirs are derived from a Monte Carlo analysis of the model, which accounts for parameter variability within expected ranges. The relationships are applied to the reservoirs in the Global Reservoirs and Dams (GRanD) database (16), to estimate the sequestration of TP and RP by dams in each of the major river basins of the world. Throughout, P retention efficiencies in a reservoir are defined asRX=Xin−XoutXin,[1]where R_X is the fractional retention of TP or RP, and X_in and X_out are the input and output fluxes of TP or RP in units of mass per unit time. Annual amounts of TP and RP retained in a reservoir are then calculated by multiplying the R_X values with the corresponding TP and RP input fluxes from the dam’s upstream watershed. The latter are obtained from the Global-NEWS-HD model, which estimates emission yields for dissolved inorganic P (DIP), dissolved organic P (DOP), and particulate P (PP), of which 20% is assumed to be reactive (7, 26). The Global-NEWS-HD yield estimates are based on the biogeophysical characteristics, population density, socioeconomic status, land use, and climatic conditions within the drainage basin (20).Because the biogeochemical mass balance model explicitly represents the in-reservoir transformations between the different forms of P, it allows us to estimate how dams modify both the total and reactive fluxes of P along rivers. With the proposed approach, we reconstruct global TP and RP retentions by dams in 1970 and 2000 and make projections for 2030. For the latter, we apply the nutrient P loading trends developed for the four Millennium Ecosystem Assessment (MEA) scenarios (27). The results illustrate the evolving role of damming in the continental P cycle and, in particular, the ongoing geographical shift in P retention resulting from the current boom in dam construction.     

Chronic liver inflammation and hepatocellular carcinogenesis are independent of S100A9

The S100A8/A9 heterodimer (calprotectin) acts as a danger signal when secreted into the extracellular space during inflammation and tissue damage. It promotes proinflammatory responses and drives tumor development in different models of inflammation‐driven carcinogenesis. S100A8/A9 is strongly expressed in several human tumors, including hepatocellular carcinoma (HCC). Apart from this evidence, the role of calprotectin in hepatocyte transformation and tumor microenvironment is still unknown. The aim of this study was to define the function of S100A8/A9 in inflammation‐driven HCC. Mice lacking S100a9 were crossed with the Mdr2^?/? model, a prototype of inflammation‐induced HCC formation. S100a9^?/? Mdr2^?/? (dKO) mice displayed no significant differences in tumor incidence or multiplicity compared to Mdr2^?/? animals. Chronic liver inflammation, fibrosis and oval cell activation were not affected upon S100a9 deletion. Our data demonstrate that, although highly upregulated, calprotectin is dispensable in the onset and development of HCC, and in the maintenance of liver inflammation.     

Effect of Periodontal Treatment in Renal Transplant Recipients

Objective

To evaluate the effect of periodontal treatment on gingival overgrowth in a group of renal transplant patients.

Subjects and Methods

Twenty-five renal transplant recipients receiving immunosuppressive therapy with cyclosporine A (CsA) were randomly assigned to 2 groups. Group 1 (n = 15) included patients who had been specifically referred to a dental clinic to prevent gingival overgrowth and were given full periodontal therapy. Group 2 (n = 10) was comprised of patients who did not receive any professional periodontal cleaning. Patients from both groups were examined to determine their periodontal status before and after 3, 6 and 12 months in terms of their plaque index, gingival index and gingival overgrowth. During the examination, their overall health was stable.

Results

For group 1, the scores were 1.89 (baseline), 0.98 (6 months) and 0.56 (12 months), and hence there were significant reductions (p = 0.0001). The gingival indices were 1.71 (baseline), 0.76 (6 months) and 0.35 (12 months), and the reductions were also significant (p = 0.0001). A significant association was observed between poor oral hygiene and the degree of gingival overgrowth. The 1-year post-treatment follow-up showed that patients in group 1 did not develop gingival overgrowth due to the use of CsA as group 2 did without prior periodontal therapy.

Conclusion

Oral hygiene status was the most important variable related to the development and degree of gingival overgrowth due to the use of CsA.Key Words: Gingival overgrowth, Periodontal treatment, Cyclosporine     

Statins enhance postischemic hyperemia in the skin circulation of hypercholesterolemic patients: a monitoring test of endothelial dysfunction for clinical practice?

OBJECTIVES: The present study aims to investigate whether laser Doppler flowmetry can be used to monitor improvements in vascular function during statin therapy. BACKGROUND: Endothelial dysfunction is an early feature of atherosclerosis in hypercholesterolemic patients and can be improved by statins. There are several methods to assess endothelial function in vivo, none of them being feasible in everyday practice. METHODS: Skin perfusion, measured by laser Doppler flowmetry, was assessed at rest and during reactive hyperemia. Nineteen hypercholesterolemic patients (age 42 to 73 years, total cholesterol 5.4 to 9.6 mmol/l) were studied before and during statin therapy. To further investigate the mechanisms, postischemic skin hyperemia was measured before and after intradermal injection of the nitric oxide synthase inhibitor L-NAME and its inactive isoform D-NAME (0.5 micromol/10 microl each). On a separate day, the healthy volunteers were reexamined before and 2 h after 1,000 mg aspirin. RESULTS: Postischemic skin blood flow was markedly reduced in hypercholesterolemic patients (45 +/- 11%) compared with healthy controls (238 +/- 20%, p < 0.0001) and improved after statin therapy (113 +/- 15%, p = 0.0005 vs. pre-treatment). In the healthy volunteers, the hyperemic responses were not significantly different after L-NAME and D-NAME. Aspirin reduced hyperemia from 274 +/- 49% to 197 +/- 40% (p = 0.025). CONCLUSIONS: Reactive hyperemia of the skin microcirculation can be easily and reproducibly assessed by laser Doppler flowmetry. Vasodilator prostaglandins are the major mediators of postischemic skin hyperemia, which is impaired in hypercholesterolemic patients and can be enhanced by cholesterol-lowering therapy. Thus, laser Doppler flowmetry may represent a tool to assess and monitor vascular function during therapy in everyday practice.     

Idiopathic CD4+ lymphocytopenia and juvenile laryngeal papillomatosis

We report on an association of idiopathic CD4+ lymphocytopenia (ICL) and juvenile laryngeal papillomatosis (JLP) in a pediatric-aged patient. Because of a past medical history of recurrent lung infections and severe chickenpox in infancy, immunologic investigations were done at age 6 years. On several occasions, a CD4+lymphocyte count of <300 cells/mm3 was detected, supporting the diagnosis of ICL. During follow-up, both medical (interferon-alpha) and surgical treatments of JLP were only partially efficient. Our patient developed disseminated infection with Mycobacterium avium and died at 10 years of age. Human papillomavirus is an important pathogen in pediatric and adult patients with ICL. In pediatric patients with JLP who develop other unusually severe viral or opportunistic infections, immunological investigations should be considered.     

Capecitabine cardiotoxicity--case reports and literature review

This study presents 3 case reports of patients who experienced anginous pain during treatment with capecitabine. The interruption of capecitabine and sublingual or intravenous nitroglycerine treatment lead to recovery. Rechallenge of capecitabine with dose reduction of 30% lead to repeated anginous pain in 2 patients. Treatment with capecitabine had been replaced with weekly bolus 5FU-LV, without further cardiotoxicity. The literature contains data from about 50 patients who experienced cardiotoxicity during capecitabine treatment. The most frequent manifestations of capecitabine cardiotoxicity included: anginous pain in 38/53 (71.7%), arrhythmia in 6/53 (11.3%), myocardial infarction in 6/53 (11.3%). Cardiotoxicity of capecitabine lead to death in 6/53 (11.3%) patients. Risk factors for cardiotoxicity are associated with the grade 4 and the fatal outcome of cardiotoxicity (p = 0.035, p = 0.015), but not with the symptom recurrence upon capecitabine rechallenge (p = 0.18). The combination chemotherapy regimens are associated with the grade 4 of cardiotoxicity (p = 0.048), but not with the fatal outcome (p = 0.3). Rechallenge of capecitabine lead to symptoms recurrence in 10/16 patients. Neither the dose reduction of capecitabine (p = 0.18) nor the additional medical prophylaxis (p = 0.37) were important for the outcome of capecitabine rechallenge.     

Impact of vasoactive intestinal polypeptide and gastrin-releasing peptide on small bowel microcirculation and mucosal injury after hepatic ischemia/reperfusion in rats

Background and aims Alterations in microvascular perfusion of the intestine after hepatic ischemia/reperfusion have been suggested as an important cause of postoperative septic complications. We therefore investigated small bowel microcirculation and mucosal injury after liver ischemia/reperfusion in a rat model. Furthermore, we analyzed the effects of the regulatory peptides vasoactive intestinal polypeptide and gastrin-releasing peptide for their splanchnic vasoactivity.Methods Hepatic ischemia was induced by clamping of the left hepatic artery and vein for 40 min, followed by 60 min of reperfusion. The control group was treated similarly, but without clamping of the liver vessels. Ten minutes after clamping of the hepatic vessels, vasoactive intestinal polypeptide or gastrin-releasing peptide, respectively, were continuously infused intravenously in the experimental groups. Small bowel microcirculation and mucosal injury were assessed using intravital microscopy and the Chiu-score, respectively.Results The functional capillary density of the small intestine following ischemia and reperfusion of the left hepatic lobe significantly decreased compared to normal controls in both the mucosa and the smooth intestinal muscle. Red blood cell velocity decreased, whereas leukocyte–endothelium adherence, stasis index and the mucosal injury score increased. Administration of vasoactive intestinal polypeptide resulted in an increase of functional capillary density in the mucosa and of the red blood cell velocity and a decrease in the stasis index. The mucosal injury score was significantly higher in reperfused animals without treatment. The application of gastrin-releasing peptide resulted in an isolated increase of the red blood cell velocity. Leukocyte adherences could not be altered by the regulatory peptides.Conclusion We conclude that hepatic ischemia/reperfusion injury leads to significant alterations of small bowel microcirculation and mucosal injury. Vasoactive intestinal polypeptide and gastrin-releasing peptide attenuate the damage in a different manner.