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We identify effective carriers of Sargassum in the Caribbean Sea and describe a mechanism for coastal choking. Revealed from satellite altimetry, the carriers of Sargassum are mesoscale eddies (vortices of 50-km radius or larger) with coherent material (i.e., fluid) boundaries. These are observer-independent—unlike eddy boundaries identified with instantaneously closed streamlines of the altimetric sea-surface height field—and furthermore harbor finite-time attractors for networks of elastically connected finite-size buoyant or "inertial" particles dragged by ocean currents and winds, a mathematical abstraction of Sargassum rafts. The mechanism of coastal inundation, identified using a minimal model of surface-intensified Caribbean Sea eddies, is thermal instability in the presence of bottom topography. [ABSTRACT FROM AUTHOR]

An increase in global wind speeds over time is affecting the global uptake of CO2 by the ocean. We determine the impact of changing winds on gas transfer and CO2 uptake by using the recently updated, global high-resolution, cross-calibrated multiplatform wind product (CCMP-V2) and a fixed monthly pCO2 climatology. In particular, we assess global changes in the context of regional wind speed changes that are attributed to large-scale climate reorganizations. The impact of wind on global CO2 gas fluxes as determined by the bulk formula is dependent on several factors, including the functionality of the gas exchange-wind speed relationship and the regional and seasonal differences in the air-water partial pressure of CO2 gradient (Δ pCO2). The latter also controls the direction of the flux. Fluxes out of the ocean are influenced more by changes in the low-to-intermediate wind speed range, while ingassing is impacted more by changes in higher winds because of the regional correlations between wind and Δ pCO2. Gas exchange-wind speed parameterizations with a quadratic and third-order polynomial dependency on wind, each of which meets global constraints, are compared. The changes in air-sea CO2 fluxes resulting from wind speed trends are greatest in the equatorial Pacific and cause a 0.03-0.04 Pg C decade−1 increase in outgassing over the 27 year time span. This leads to a small overall decrease of 0.00 to 0.02 Pg C decade−1 in global net CO2 uptake, contrary to expectations that increasing winds increase net CO2 uptake. [ABSTRACT FROM AUTHOR]

Objective: Diabetes may accelerate atheromatosis in uremic patients. Our aim was to assess the influence of type 1 diabetes on the atheromatosis-related inflammation in patients with chronic kidney disease (CKD).Research Design and Methods: We analyzed the expression of proinflammatory cytokines and adhesion molecules in the inferior epigastric artery walls of type 1 diabetic patients with CKD (n = 22) and compared it with nondiabetic uremic patients (n = 92) at the time of kidney transplantation. We evaluated the expression of interleukin (IL)-6, monocyte chemotractant protein (MCP)-1, vascular cell adhesion molecule (VCAM)-1, intercellular adhesion molecule-1, and the activation of nuclear factor-κβ p65 (NFkB-p65). Common carotid intima-media thickness (c-IMT) was determined by conventional echography.Results: IL-6, MCP-1, and VCAM-1 proteins were elevated in type 1 diabetic patients compared with nondiabetic subjects (P < 0.05). The nuclear localization of NFkB-p65 was higher in type 1 diabetic patients (P < 0.01) and correlated with the levels of MCP-1 in this group (r = 0.726, P < 0.001). Arterial fibrosis correlated with IL-6 and MCP-1 levels (r = 0.411, P < 0.001 and r = 0.378, P = 0.001). A significant correlation was observed between VCAM-1 levels and both the degree of arterial narrowing and c-IMT.Conclusions: Type 1 diabetes produces a proinflammatory state in the arteries of end-stage CKD patients, with increased levels of IL-6, MCP-1, and VCAM-1, as well as a greater degree of p65 activation, which are associated with more severe vascular lesions and higher c-IMT. Although causality is not demonstrated, these findings support the major role of inflammation in type 1 diabetic patients with CKD. [ABSTRACT FROM AUTHOR]

Competing Interests: Declaration of interests VK and OS are staff members of the WHO Regional Office for Europe. The authors alone are responsible for the views expressed in this publication and they do not necessarily represent the decisions or policies of WHO. The designations employed and the presentation of the material in this publication do not imply the expression of any opinion whatsoever on the part of WHO concerning the legal status of any country, territory, city, or area or of its authorities, or concerning the delimitation of its frontiers or boundaries. Dotted and dashed lines on maps represent approximate border lines for which there might not yet be full agreement. AK and EV are staff members of the European Environment Agency. The views expressed in this article are solely those of the authors and its content does not necessarily represent the views or position of the European Environment Agency. All other authors declare no competing interests.

Competing Interests: Declaration of interests CD was supported by the UK Natural Environment Research Council (NE/R010811/1) and the UK Natural Environment Research Council Independent Research Fellowship (NE/N01524X/1) and contributes to the Sustainable and Healthy Food Systems project supported by the Wellcome Trust (205200/Z/16/Z). MD was supported by the Wellcome Trust's Complex Urban Systems for Sustainability and Health (CUSSH) project (209387/Z/17/Z). YL was supported by the US National Aeronautics and Space Administration Applied Sciences Program (80NSSC21K0507). RL was supported by a Royal Society Dorothy Hodgkin Fellowship. MSo was supported by Horizon 2020 project EXHAUSTION (820655) and Academy of Finland HEATCOST (334798). SHG and JKWL were supported by Singapore's National Research Foundation, Singapore's Prime Minister's Office, under its Campus for Research Excellence and Technological Enterprise programme. IH was supported by the UK Research and Innovation (UKRI) Engineering and Physical Sciences Research Council Centre for Research in Energy Demand Solutions (EP/R035288/1) and UKRI APEx (NE/T001887/1). JM was supported by the German Ministry for Education and Research (01LA1826A and 03SFK5J0). ML was supported by the Sloan Foundation. All other authors declare no competing interests.

Competing Interests: Declaration of interests VK and OS are staff members of the WHO Regional Office for Europe. The authors alone are responsible for the views expressed in this publication and they do not necessarily represent the decisions or policies of the World Health Organization. The designations employed and the presentation of the material in this publication do not imply the expression of any opinion whatsoever on the part of WHO concerning the legal status of any country, territory, city or area or of its authorities, or concerning the delimitation of its frontiers or boundaries. Dotted and dashed lines on maps represent approximate border lines for which there may not yet be full agreement. All other authors declare no competing interests.

Translations: For the Chinese, French, German, and Spanish translations of the abstract see Supplementary Materials section., (Copyright © 2021 Elsevier Ltd. All rights reserved.)

Active maintenance of β-cell identity through fine-tuned regulation of key transcription factors ensures β-cell function. Tacrolimus, a widely used immunosuppressant, accelerates onset of diabetes after organ transplantation, but underlying molecular mechanisms are unclear. Here we show that tacrolimus induces loss of human β-cell maturity and β-cell failure through activation of the BMP/SMAD signaling pathway when administered under mild metabolic stress conditions. Tacrolimus-induced phosphorylated SMAD1/5 acts in synergy with metabolic stress-activated FOXO1 through formation of a complex. This interaction is associated with reduced expression of the key β-cell transcription factor MAFA and abolished insulin secretion, both in vitro in primary human islets and in vivo in human islets transplanted into high-fat diet-fed mice. Pharmacological inhibition of BMP signaling protects human β-cells from tacrolimus-induced β-cell dysfunction in vitro. Furthermore, we confirm that BMP/SMAD signaling is activated in protocol pancreas allograft biopsies from recipients on tacrolimus. To conclude, we propose a novel mechanism underlying the diabetogenicity of tacrolimus in primary human β-cells. This insight could lead to new treatment strategies for new-onset diabetes and may have implications for other forms of diabetes., (© 2019 by the American Diabetes Association.)

Ocean flows are routinely inferred from low-resolution satellite altimetry measurements of sea surface height assuming a geostrophic balance. Recent nonlinear dynamical systems techniques have revealed that surface currents derived from altimetry can support mesoscale eddies with material boundaries that do not filament for many months, thereby representing effective transport mechanisms. However, the long-range Lagrangian coherence assessed for mesoscale eddy boundaries detected from altimetry is constrained by the impossibility of current altimeters to resolve ageostrophic submesoscale motions. These may act to prevent Lagrangian coherence from manifesting in the rigorous form described by the nonlinear dynamical systems theories. Here we use a combination of satellite ocean color and surface drifter trajectory data, rarely available simultaneously over an extended period of time, to provide observational evidence for the enduring Lagrangian coherence of a Loop Current ring detected from altimetry. We also seek indications of this behavior in the flow produced by a data-assimilative system which demonstrated ability to reproduce observed relative dispersion statistics down into the marginally submesoscale range. However, the simulated flow, total surface and subsurface or subsampled emulating altimetry, is not found to support the long-lasting Lagrangian coherence that characterizes the observed ring. This highlights the importance of the Lagrangian metrics produced by the nonlinear dynamical systems tools employed here in assessing model performance.

Kidney transplant (KT) is the treatment of choice for most patients with chronic kidney disease, but this has a high cardiovascular mortality due to traditional and nontraditional risk factors, including vascular calcification. Inflammation could precede the appearance of artery wall lesions, leading to arteriosclerosis and clinical and subclinical atherosclerosis in these patients. Additionally, mineral metabolism disorders and activation of the renin-angiotensin system could contribute to this vascular damage. Thus, understanding the vascular lesions that occur in KT recipients and the pathogenic mechanisms involved in their development could be crucial to optimize the therapeutic management and outcomes in survival of this population. This review focuses on the following issues: (1) epidemiological data framing the problem; (2) atheromatosis in KT patients: subclinical and clinical atheromatosis, involving ischemic heart disease, congestive heart failure, stroke and peripheral vascular disease; (3) arteriosclerosis and vascular calcifications; and (4) potential pathogenic mechanisms and their therapeutic targets., (Copyright © 2017 Southern Society for Clinical Investigation. Published by Elsevier Inc. All rights reserved.)

Introduction: Matrix metalloproteinases (MMPs) are overexpressed at different stages of colorectal carcinogenesis and could serve as early surrogate biomarkers of colorectal neoplasia., Objective: To assess the utility of plasma MMP2 and MMP9 levels in the detection of advanced colorectal neoplasia and their correlation with tissue levels., Methods: We analysed blood and tissue samples from patients with non-advanced adenomas (n=25), advanced adenomas (n=25), colorectal cancer (n=25) and healthy controls (n=75). Plasma and tissue gelatinase levels were determined by Luminex XMAP technology and gelatin zymography. Receiver operating characteristic (ROC) curve analysis was used to calculate the optimum cut-off for the detection of advanced colorectal neoplasia., Results: Plasma MMP2 levels were similar between groups whatever the type of lesion. Plasma MMP9 levels were significantly higher in patients with neoplastic lesions than in healthy controls (median 292.3ng/ml vs. 139.08ng/ml, P<0.001). MMP9 levels were also higher in colorectal cancer than in non-advanced adenomas (median 314.6ng/ml vs. 274.3ng/ml, P=0.03). There was a significant correlation between plasma and tissue levels of MMP9 (r=0.5, P<0.001). The plasma MMP9 cut-off range with the highest diagnostic accuracy was between 173ng/ml and 204ng/ml (AUC=0.80 [95% CI: 0.72-0.86], P<0.001; sensitivity, 80-86% and specificity, 57-67%)., Conclusion: Plasma MMP9 could be a surrogate biomarker for the early detection of advanced colorectal neoplasia, although its diagnostic performance could be increased by combination with other biomarkers., (Copyright © 2015 Elsevier España, S.L.U. y AEEH y AEG. All rights reserved.)

Recent developments in dynamical systems theory have revealed long-lived and coherent Lagrangian (i.e., material) eddies in incompressible, satellite-derived surface ocean velocity fields. Paradoxically, observed drifting buoys and floating matter tend to create dissipative-looking patterns near oceanic eddies, which appear to be inconsistent with the conservative fluid particle patterns created by coherent Lagrangian eddies. Here, we show that inclusion of inertial effects (i.e., those produced by the buoyancy and size finiteness of an object) in a rotating two-dimensional incompressible flow context resolves this paradox. Specifically, we obtain that anticyclonic coherent Lagrangian eddies attract (repel) negatively (positively) buoyant finite-size particles, while cyclonic coherent Lagrangian eddies attract (repel) positively (negatively) buoyant finite-size particles. We show how these results explain dissipative-looking satellite-tracked surface drifter and subsurface float trajectories, as well as satellite-derived Sargassum distributions.

Background: Kidney transplant recipients have high cardiovascular risk, and vascular inflammation may play an important role. We explored whether the inflammatory state in the vessel wall was related to carotid intima-media thickness (c-IMT) and patient survival following kidney transplantation., Methods: In this prospective observational cohort study we measured c-IMT and expression of proinflammatory cytokines and adhesion molecules in the inferior epigastric artery in 115 kidney transplant candidates. Another c-IMT measurement was done 1-year post-transplantation in 107. By stepwise multiple regression analysis we explored factors associated with baseline c-IMT and their changes over time. Multivariate Cox regression analysis was constructed to identify risk factors for mortality., Results: A worse cardiovascular profile (older age, smoker, diabetic, carotid plaque, systolic blood pressure and vascular calcification) and higher VCAM-1 levels were found in patients in the highest baseline c-IMT tertile, who also had a worse survival. Factors independently related to baseline c-IMT were age (β=0.369, P<0.0001), fasting glucose (β=0.168, P=0.045), smoking (β=0.228, P=0.003) and VCAM-1 levels (β=0.244, P=0.002). Independent factors associated with c-IMT measurement 1-year post-transplantation were baseline c-IMT (β=-0.677, P<0.0001), post-transplant diabetes (β=0.225, P=0.003) and triglycerides (β=0.302, P=0.023). Vascular VCAM-1 levels were associated with increased risk of mortality in bivariate and multivariate Cox regression. Notably, nearly 50% of patients showed an increase or maintenance of high c-IMT 1 year post-transplantation and these patients experienced a higher mortality (13 versus 3.5%; P=0.021)., Conclusion: A worse cardiovascular profile and a higher vascular VCAM-1 protein levels at time of KT are related to subclinical atheromatosis. This could lead to a higher post-transplant mortality. Pre-transplant c IMT, post-transplant diabetes and triglycerides at 1-year post-transplantation may condition a high c-IMT measurement post-transplantation, which may decrease patient survival.

Background: Switching to cyclosporine A may result in a reversion of tacrolimus-induced diabetes mellitus. However, mechanisms underlying such a reversion are still unknown., Methods: Obese Zucker rats were used as a model for tacrolimus-induced diabetes mellitus. A cohort of 44 obese Zucker rats received tacrolimus for 11 days (0.3mg/kg/day) until diabetes development; then: (a)22 rats were euthanized at day 12 and were used as a reference group (tacrolimus-day 12), and (b)22 rats on tacrolimus were shifted to cyclosporin (2.5mg/kg/day) for 5 days (tacrolimus-cyclosporin). An additional cohort of 22 obese Zucker rats received the vehicle for 17 days and were used as a control group. All animals underwent an intraperitoneal glucose tolerance test at the end of the study., Results: β-cell proliferation, apoptosis and Ins2 gene expression were evaluated. Compared to rats in tacrolimus-day 12 group, those in tacrolimus-cyclosporin group showed a significant improvement in blood glucose levels in all assessment points in intraperitoneal glucose tolerance test. Diabetes decreased from 100% in tacrolimus-day 12 group to 50% in tacrolimus-cyclosporin group. Compared to tacrolimus-day 12 group, rats in tacrolimus-cyclosporin group showed an increased β-cell proliferation, but such an increase was lower than in rats receiving the vehicle. Ins2 gene expressions in rats receiving tacrolimus-cyclosporin and rats receiving the vehicle were comparable., Conclusion: An early switch from tacrolimus to cyclosporin in tacrolimus-induced diabetes mellitus resulted in an increased β-cell proliferation and reversion of diabetes in 50% of cases., (Copyright © 2015 The Authors. Published by Elsevier España, S.L.U. All rights reserved.)

The dynamics of dissemination of the environmental human pathogen Vibrio parahaemolyticus are uncertain. The O3:K6 clone was restricted to Asia until its detection along the Peruvian coasts and in northern Chile in 1997 in phase with the arrival of El Niño waters. A subsequent emergence of O3:K6 strains was detected in austral Chile in 2004. The origin of these 1997 and 2004 population radiations has not yet been conclusively determined. Multiple loci VNTR analysis using seven polymorphic loci was carried out with a number of representative strains from Asia, Peru and Chile to determine their genetic characteristics and population structure. Asian and Chilean subpopulations were the most genetically distant groups with an intermediate subpopulation in Peru. Population structure inferred from a minimum-spanning tree and Bayesian analysis divided the populations into two genetically distinct groups, consistent with the epidemic dynamics of the O3:K6 clone in South America. One group comprised strains from the original Asiatic population and strains arriving in Peru and Chile in 1997. The second group included the remaining Peruvian Strains and Chilean strains obtained from Puerto Montt in 2004. The analysis of the arrival of the O3:K6 clone at the Pacific coasts of South America has provided novel insights linking the origin of the invasion in 1997 to Asian populations and describing the successful establishment of the O3:K6 populations, first in Peru and subsequently in the South of Chile owing to a possible radiation of Peruvian populations., (© 2010 Blackwell Publishing Ltd.)

Five cases of duodenal obstruction due to biliary stones (Bouveret's syndrome) are reported. Presenting symptoms were gastric outlet obstruction, upper gastrointestinal bleeding or jaundice. Diagnosis was achieved either by endoscopy, upper gastrointestinal X-Ray series or at the operating room. Surgical procedures to remove obstruction were needed in every case: cholecystectomy was simultaneously performed on two occasions. After reviewing the literature, previous biliary symptoms were found in 65% of the cases; diagnosis was achieved preoperatively in 85%, mainly by endoscopy procedures; simultaneous cholecystectomy was carried out in 56% of cases; postoperative mortality was 24%, rising when simultaneous cholecystectomy was performed.