The Gulf of Aden Intermediate Water Intrusion Regulates the Southern Red Sea Summer Phytoplankton Blooms

Knowledge on large-scale biological processes in the southern Red Sea is relatively limited, primarily due to the scarce in situ, and satellite-derived chlorophyll-a (Chl-a) datasets. During summer, adverse atmospheric conditions in the southern Red Sea (haze and clouds) have long severely limited the retrieval of satellite ocean colour observations. Recently, a new merged ocean colour product developed by the European Space Agency (ESA)Ðthe Ocean Color Climate Change Initiative (OC-CCI)Ðhas substantially improved the southern Red Sea coverage of Chl-a, allowing the discovery of unexpected intense summer blooms. Here we provide the first detailed description of their spatiotemporal distribution and report the mechanisms regulating them. During summer, the monsoon-driven wind reversal modifies the circulation dynamics at the Bab-el-Mandeb strait, leading to a subsurface influx of colder, fresher, nutrient-rich water from the Indian Ocean. Using satellite observations, model simulation outputs, and in situ datasets, we track the pathway of this intrusion into the extensive shallow areas and coral reef complexes along the basin's shores. We also provide statistical evidence that the subsurface intrusion plays a key role in the development of the southern Red Sea phytoplankton blooms

Sensing coral reef connectivity pathways from space

Coral reefs rely on inter-habitat connectivity to maintain gene flow, biodiversity and ecosystem resilience. Coral reef communities of the Red Sea exhibit remarkable genetic homogeneity across most of the Arabian Peninsula coastline, with a genetic break towards the southern part of the basin. While previous studies have attributed these patterns to environmental heterogeneity, we hypothesize that they may also emerge as a result of dynamic circulation flow; yet, such linkages remain undemonstrated. Here, we integrate satellite-derived biophysical observations, particle dispersion model simulations, genetic population data and ship-borne in situ profiles to assess reef connectivity in the Red Sea. We simulated long-term (>20 yrs.) connectivity patterns driven by remotely-sensed sea surface height and evaluated results against estimates of genetic distance among populations of anemonefish, Amphiprion bicinctus, along the eastern Red Sea coastline. Predicted connectivity was remarkably consistent with genetic population data, demonstrating that circulation features (eddies, surface currents) formulate physical pathways for gene flow. The southern basin has lower physical connectivity than elsewhere, agreeing with known genetic structure of coral reef organisms. The central Red Sea provides key source regions, meriting conservation priority. Our analysis demonstrates a cost-effective tool to estimate biophysical connectivity remotely, supporting coastal management in data-limited regions

Pharmacological targeting of NF-κB potentiates the effect of the topoisomerase inhibitor CPT-11 on colon cancer cells

NF-κB interferes with the effect of most anti-cancer drugs through induction of anti-apoptotic genes. Targeting NF-κB is therefore expected to potentiate conventional treatments in adjuvant strategies. Here we used a pharmacological inhibitor of the IKK2 kinase (AS602868) to block NF-κB activation. In human colon cancer cells, inhibition of NF-κB using 10 μM AS602868 induced a 30–50% growth inhibitory effect and strongly enhanced the action of SN-38, the topoisomerase I inhibitor and CPT-11 active metabolite. AS602868 also potentiated the cytotoxic effect of two other antineoplasic drugs: 5-fluorouracil and etoposide. In xenografts experiments, inhibition of NF-κB potentiated the antitumoural effect of CPT-11 in a dose-dependent manner. Eighty-five and 75% decreases in tumour size were observed when mice were treated with, respectively, 20 or 5 mg kg−1 AS602868 associated with 30 mg kg−1 CPT-11 compared to 47% with CPT-11 alone. Ex vivo tumour analyses as well as in vitro studies showed that AS602868 impaired CPT-11-induced NF-κB activation, and enhanced tumour cell cycle arrest and apoptosis. AS602868 also enhanced the apoptotic potential of TNFα on HT-29 cells. This study is the first demonstration that a pharmacological inhibitor of the IKK2 kinase can potentiate the therapeutic efficiency of antineoplasic drugs on solid tumours

An adiponectin-like molecule with antidiabetic properties

Adiponectin increases glucose transport, reduces inflammation, and controls vascular functions. Hence, we propose that treatment with a recombinant globular domain of adiponectin (rgAd110-244) has significant therapeutic potential to treat insulin resistance. Mice were fed for 3 months on a high-fat diet (HFD) to induce insulin resistance, diabetes, and moderate weight gain. The mice were first infused iv with different doses of rgAd110-244 (0.12, 0.4, and 1.2 microg/kg x min) for 5 h. Basal and insulin-sensitive glucose use rates were assessed by the use of a submaximal rate of insulin in the awake free-moving mouse. rgAd110-244 reduced, with dose dependence, epinephrine-induced hyperglycemia and HFD-induced insulin resistance by increasing whole-body glucose use (35% at the highest dose) and glycolysis rates. Similarly, the reduction of plasma free fatty acid concentrations by insulin was dramatically improved. Basal hepatic glucose production was unchanged by rgAd110-244 infusion. This acute rgAd110-244 treatment improved glucose homeostasis and was associated with an increased content of muscle phospho-Akt, glycogen synthase kinase-3beta, and AMP-activated kinase. Second, HFD mice were chronically treated with sc rgAd110-244 injections (10, 30, and 100 microg/kg). Fasting glycemia and insulin-sensitive glucose use were improved by rgAd110-244 at the highest dose at completion of the treatment, with concomitant reduction in body weight gain. We here show for the first time that a recombinant adiponectin fragment (110-244 amino acids called rgAd110-244) is able to treat insulin-resistant diabetes. Our results strongly suggest further pharmacological investigation of rgAd110-244 with the objective of developing a new treatment of insulin-resistant diabetes

Regulation of FADS2 expression and activity in European sea bass (Dicentrarchus labrax, L.) fed a vegetable diet

Supplies of marine fish oils are limited, and continued growth in aquaculture production dictates that lipid substitutes in fish diets must be used without compromising fish health and product quality. In this study, the total substitution of a fish meal and fish oil by a blend of vegetable meals (corn, soybean, wheat and lupin) and linseed oil in the diet of European sea bass (Dicentrachus labrax) was investigated. Two groups of European sea bass were fed with fish diet (FD) or vegetable diet (VD) for 9 months. VD, totally deprived of eicosapentaenoate (EPA; 20:5n-3) and docosahexaenoate (DHA; 22:6n-3), revealed a nutritional deficiency and affected growth performance. Whilst VD induced a significant increase in fatty acid desaturase 2 (FADS2) and sterol binding regulatory element-binding protein 1 (SREBP-1) mRNA levels, the desaturation rate of [1-C-14]18:3n-3 into [1-C-14]18:4n-3, analysed in microsomal preparations using HPLC method, did not show an upregulation of FADS2 activities in liver and intestine of fish fed VD. Moreover Western-blot analysis did not revealed any significant difference of FADS2 protein amount between the two dietary groups. These data demonstrate that sea bass exhibits a desaturase (FADS2) activity whatever their diet, but a post-transcriptional regulation of fads2 RNA prevents an increase of enzyme in fish fed a HUFA-free diet. This led to a lower fish growth and poor muscle HUFA content

Estimating model error covariances in nonlinear state-space models using Kalman smoothing and the expectation-maximisation algorithm

International audienceSpecification and tuning of errors from dynamical models are important issues in data assimilation. In this work, we propose an iterative expectation-maximization (EM) algorithm to estimate the model-error covariances using classical extended and ensemble versions of the Kalman smoother. We show that, for additive model errors, the estimate of the error covariance converges. We also investigate other forms of model error, such as parametric or multiplicative errors. We show that additive Gaussian model error is able to compensate for non-additive sources of error in the algorithms we propose. We also demonstrate the limitations of the extended version of the algorithm and recommend the use of the more robust and flexible ensemble version. This article is a proof of concept of the methodology with the Lorenz-63 attractor. We developed an open-source Python library to enable future users to apply the algorithm to their own nonlinear dynamical models