Seagrass beds are highly productive coastal ecosystems providing a large array of ecosystem services including fisheries and carbon sequestration. As seagrasses are known to be highly sensitive to ...anthropogenic forcing, we evaluated the use of trace metal concentrations in seagrasses as bioindicators for trace metal pollution of coastal regions at both global and local scale. We carried out a meta-analysis based on literature data to provide a global benchmark list for trace metal accumulation in seagrasses, which was lacking in literature. We subsequently carried out a case study at the Caribbean islands of Curaçao and Bonaire to test for local-scale differences in trace metal concentrations in seagrasses, and internal metal allocation. The benchmark and local study show that trace metal concentrations in seagrass leaves, regardless of the species, can vary over a 100-1000-fold range, and are related to the level of anthropogenic pressure, making seagrasses highly valuable indicators.
•We studied the nutrient status of the poorly studied Caribbean seagrass beds.•We identified imminent threats from eutrophication to seagrasses on Curaçao & Bonaire.•Leaf nutrients of Thalassia ...testudinum can be used as point source indicators.•Sewage discharge and coastal residential areas are point sources of eutrophication.•Measures should be taken to prevent seagrass loss on Curaçao due to eutrophication.
Seagrass beds are globally declining due to human activities in coastal areas. We here aimed to identify threats from eutrophication to the valuable seagrass beds of Curaçao and Bonaire in the Caribbean, which function as nursery habitats for commercial fish species. We documented surface- and porewater nutrient concentrations, and seagrass nutrient concentrations in 6 bays varying in nutrient loads. Water measurements only provided a momentary snapshot, due to timing, tidal stage, etc., but Thalassia testudinum nutrient concentrations indicated long-term nutrient loads. Nutrient levels in most bays did not raise any concern, but high leaf % P values of Thalassia in Piscadera Bay (∼0.31%) and Spanish Water Bay (∼0.21%) showed that seagrasses may be threatened by eutrophication, due to emergency overflow of waste water and coastal housing. We thus showed that seagrasses may be threatened and measures should be taken to prevent loss of these important nursery areas due to eutrophication.
•We studied effects of high sediment nutrient and organic loading on seagrass patches.•High sulfide and ammonium levels impaired patch survival and expansion.•Sulfide concentrations >1000μmolL−1 were ...toxic to mother patch and expansion.•Ammonium concentrations >2000μmolL−1 decreased patch expansion.•Mother patches were less affected by high ammonium due to joint detoxification.
As a result of anthropogenic disturbances and natural stressors, seagrass beds are often patchy and heterogeneous. The effects of high loads of nutrients and organic matter in patch development and expansion in heterogeneous seagrass beds have, however, poorly been studied. We experimentally assessed the in situ effects of sediment quality on seagrass (Zostera noltii) patch dynamics by studying patch (0.35m diameter) development and expansion for 4 sediment treatments: control, nutrient addition (NPK), organic matter addition (OM) and a combination (NPK+OM). OM addition strongly increased porewater sulfide concentrations whereas NPK increased porewater ammonium, nitrate and phosphate concentrations. As high nitrate concentrations suppressed sulfide production in NPK+OM, this treatment was biogeochemically comparable to NPK. Sulfide and ammonium concentrations differed within treatments, but over a 77 days period, seagrass patch survival and expansion were impaired by all additions compared to the control treatment. Expansion decreased at porewater ammonium concentrations >2000μmolL−1. Mother patch biomass was not affected by high porewater ammonium concentrations as a result of its detoxification by higher seagrass densities. Sulfide concentrations >1000μmolL−1 were toxic to both patch expansion and mother patch. We conclude that patch survival and expansion are constrained at high loads of nutrients or organic matter as a result of porewater ammonium or sulfide toxicity.
In recent years it has become clear that many extra-uterine (pelvic) high-grade serous carcinomas (serous carcinomas) are preceded by a precursor lesion in the distal fallopian tube. Precursors range ...from small self-limited ‘p53 signatures' to expansile serous tubal intraepithelial neoplasms that include both serous tubal epithelial proliferations (or lesions) of uncertain significance and serous tubal intraepithelial carcinomas. These precursors can be considered from three perspectives. The first is biologic underpinnings, which are multifactorial, and include the intersection of DNA damage with Tp53 mutations and disturbances in transcriptional regulation that increase with age. The second perspective is the morphologic discovery and classification of intraepithelial neoplasms that are intercepted early in their natural history, either incidentally or in risk-reduction surgeries for germline mutations. For the practicing pathologist, as well as the investigators, a distinction between a primary intraepithelial neoplasm and an intramucosal carcinoma must be made to avoid misinterpreting (or underestimating) the significance of these proliferations. The third perspective is the application of this information to intervention, devising strategies that will actually lower the ovarian cancer death rate by opportunistic salpingectomy, widespread comprehensive genetic screening and early detection. Central to this issue are the questions of (1) whether some STICs are metastatic, (2) whether lower-grade epithelial proliferations can invade prior to evolving into intraepithelial carcinoma, or (3) metastasize and become malignant elsewhere (‘precursor escape'). An important caveat is the persistent and unsettling reality that many high-grade serous carcinomas are not associated with an obvious point of initiation in the fallopian tube. The pathologist sits squarely in the midst of all of these issues, and has a pivotal role in managing expectations for stemming the death rate from this lethal disease.
Hereditary deficiencies of protein S, protein C and antithrombin are known risk factors for first venous thromboembolism. We assessed the absolute risk of recurrence, and the contribution of ...concomitant thrombophilic defects in a large cohort of families with these deficiencies. Annual incidence of recurrence was estimated in 130 deficient patients, with separate estimates for those with each of protein S, protein C, and antithrombin deficiency, and in eight non-deficient patients with prior venous thromboembolism. All patients were also tested for factor V Leiden, prothrombin G20210A, high levels of factors VIII, IX and XI, and hyperhomocysteinemia. There were 81 recurrent events among 130 deficient patients. Median follow-up was 4.6 years. Annual incidences (95% confidence interval) of recurrent venous thromboembolism were 8.4% (5.8-11.7) for protein S deficiency, 6.0% (3.9-8.7) for protein C deficiency, 10.0% (6.1-15.4) for antithrombin deficiency, and overall 7.7% (6.1-9.5). Relative risk of recurrence in patients with a spontaneous versus provoked first event was 1.5 (0.95-2.3). Cumulative recurrence rates at 1, 5 and 10 years were 15%, 38% and 53%. Relative risk of recurrence with concomitant defects was 1.4 (0.7-2.6) (1 defect) and 1.4 (0.8-2.7) (> or =2 defects). Annual incidence was 1.0% (0.03-5.5) in eight non-deficient patients. Annual incidence of major bleeding in deficient patients on oral anticoagulant treatment was 0.5% (0.2-1.0). We conclude that patients with a hereditary protein S, protein C or antithrombin deficiency appear to have a high absolute risk of recurrence. This risk is increased after a first spontaneous event, and by concomitance of other thrombophilic defects.
No data are available on the absolute risk of either venous thromboembolism (VTE) or arterial thromboembolism (ATE) in patients with nephrotic syndrome. Reported risks are based on multiple case ...reports and small studies with mostly short-term follow-up. We assessed the absolute risk of VTE and ATE in a large, single-center, retrospective cohort study and attempted to identify predictive factors in these patients.
A total of 298 consecutive patients with nephrotic syndrome (59% men; mean age, 42+/-18 years) were enrolled. Mean follow-up was 10+/-9 years. Nephrotic syndrome was defined by proteinuria > or =3.5 g/d, and patients were classified according to underlying histological lesions accounting for nephrotic syndrome. Objectively verified symptomatic thromboembolic events were the primary study outcome. Annual incidences of VTE and ATE were 1.02% (95% confidence interval, 0.68 to 1.46) and 1.48% (95% confidence interval, 1.07 to 1.99), respectively. Over the first 6 months of follow-up, these rates were 9.85% and 5.52%, respectively. Proteinuria and serum albumin levels tended to be related to VTE; however, only the predictive value of the ratio of proteinuria to serum albumin was significant (hazard ratio, 5.6; 95% confidence interval, 1.2 to 26.2; P=0.03). In contrast, neither the degree of proteinuria nor serum albumin levels were related to ATE. Sex, age, hypertension, diabetes, smoking, prior ATE, and estimated glomerular filtration rate predicted ATE (P< or =0.02).
This study verifies high absolute risks of symptomatic VTE and ATE that were remarkably elevated within the first 6 months. Whereas the ratio of proteinuria to serum albumin predicted VTE, estimated glomerular filtration rate and multiple classic risk factors for atherosclerosis were predictors of ATE.
A novel electrochemical (EC) method for fast and efficient reduction of the disulfide bonds in proteins and peptides is presented. The method does not use any chemical agents and is purely ...instrumental. To demonstrate the performance of the EC reactor cell online with electrospray mass spectrometry, insulin and somatostatin were used as model compounds. Efficient reduction is achieved in continuous infusion mode using an EC reactor cell with a titanium-based working electrode. Under optimized conditions, the presented method shows almost complete reduction of insulin and somatostatin. The method does not require any special sample preparation, and the EC reactor cell makes it suitable for automation. Online EC reduction followed by collision-induced dissociation fragmentation of somatostatin showed more backbone cleavages and improved sequence coverage. By adjusting the settings, the EC reaction efficiency was gradually changed from partial to full disulfide bonds reduction in α-lactalbumin, and the expected shift in charge state distribution has been demonstrated. The reduction can be controlled by adjusting the square-wave pulse, flow rate or mobile phase composition. We have shown the successful use of an EC reactor cell for fast and efficient reduction of disulfide bonds for online mass spectrometry of proteins and peptides. The possibility of online and gradual disulfide bond reduction adds a unique dimension to characterization of disulfide bonds in mid- and top-down proteomics applications.
Figure
Principle of electrochemical reduction of disulfide bonds in proteins
Thrombophilia screening is controversial. In a retrospective family cohort, where probands had thrombosis and a thrombophilic defect, 2479 relatives were tested for thrombophilia. In antithrombin-, ...protein C–, and protein S–deficient relatives, annual incidences of venous thrombosis were 1.77% (95% CI, 1.14-2.60), 1.52% (95% CI, 1.06-2.11), and 1.90% (95% CI, 1.32-2.64), respectively, at a median age of 29 years and a positive family history of more than 20% symptomatic relatives. In relatives with factor V (FV) Leiden, prothrombin 20210G>A, or high FVIII levels, these were 0.49% (95% CI, 0.39-0.60), 0.34% (95% CI, 0.22-0.49), and 0.49% (95% CI, 0.41-0.51), respectively. High FIX, FXI, and TAFI, and hyperhomocysteinemia were not independent risk factors. Annual incidence of major bleeding in antithrombin-, protein C–, or protein S–deficient relatives on anticoagulants was 0.29% (95% CI, 0.03-1.04). Cumulative recurrence rates in relatives with antithrombin, protein C, or protein S deficiency were 19% at 2 years, 40% at 5 years, and 55% at 10 years. In relatives with FV Leiden, prothrombin 20210G>A, or high levels FVIII, these were 7%, 11%, and 25%, respectively. Considering its clinical implications, thrombophilia testing should address hereditary deficiencies of antithrombin, protein C, and protein S in patients with first venous thrombosis at young age and/or a strong family history of venous thrombosis.
This paper focuses on the regulation of prostitution in the Netherlands from the twentieth century onward. It aims to provide a full description of the Dutch position on prostitution through the ...interpretation and explanation of current Dutch prostitution policy. This will be achieved by analyzing the legal narratives that substantiate the legal rules provided in both Dutch criminal and administrative law concerning the regulation of prostitution. We analyze the Dutch prostitution legislation of the past, present, and future, using a newly developed analytical framework. Using this framework, we reconstruct the legislator’s attitude towards prostitution using insights from previous theoretical work on prostitution and using models aimed at regulating this phenomenon that range from a total ban to full decriminalization. In our analysis, we also use the legitimating grounds for application of criminal law developed by Feinberg. These grounds are also used in this paper to interpret the administrative intervention in prostitution. This paper reveals a paradox: The idea of a liberal dream goes hand-in-hand with growing repression of freedom in the Dutch prostitution sector.
Whether hereditary protein S, protein C, or antithrombin deficiency is associated with arterial thromboembolism (ATE) and whether history of venous thromboembolism in these subjects predisposes them ...to subsequent ATE have yet to be determined.
On the basis of pedigree analysis, we enrolled a total of 552 subjects (52% women; mean age, 46+/-17 years), belonging to 84 different kindreds, in this retrospective family cohort study. Detailed information on previous episodes of venous thromboembolism, ATE, anticoagulant use, and atherosclerosis risk factors was collected. Primary study outcome was objectively verified symptomatic ATE. Of 552 subjects, 308 had protein S (35%), protein C (39%), or antithrombin (26%) deficiency. Overall, annual incidences of ATE were 0.34% (95% confidence interval CI, 0.23 to 0.49) in deficient versus 0.17% (95% CI, 0.09 to 0.28) in nondeficient subjects; the hazard ratio was 2.3 (95% CI, 1.2 to 4.5). Because the risk hazards varied over lifetime, we performed a time-dependent analysis. After adjusting for atherosclerosis risk factors and clustering within families, we found that deficient subjects had a 4.7-fold (95% CI, 1.5 to 14.2; P=0.007) higher risk for ATE before 55 years of age versus 1.1 (95% CI, 0.5 to 2.6) thereafter compared with nondeficient family members. For separate deficiencies, the risks were 4.6- (95% CI, 1.1 to 18.3), 6.9- (95% CI, 2.1 to 22.2), and 1.1- (95% CI, 0.1 to 10.9) fold higher in protein S-, protein C-, and antithrombin-deficient subjects, respectively, before 55 years of age. History of venous thromboembolism was not related to subsequent ATE (hazard ratio, 1.1; 95% CI, 0.5 to 2.2).
Compared with nondeficient family members, subjects with protein S or protein C deficiency but not antithrombin deficiency have a higher risk for ATE before 55 years of age that is independent of prior venous thromboembolism.
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