On-Line Identification of Autonomous Underwater Vehicles through Global Derivative-Free Optimization

We describe the design and implementation of an on-line identification scheme for Autonomous Underwater Vehicles (AUVs). The proposed method estimates the dynamic parameters of the vehicle based on a global derivative-free optimization algorithm. It is not sensitive to initial conditions, unlike other on-line identification schemes, and does not depend on the differentiability of the model with respect to the parameters. The identification scheme consists of three distinct modules: a) System Excitation, b) Metric Calculator and c) Optimization Algorithm. The System Excitation module sends excitation inputs to the vehicle. The Optimization Algorithm module calculates a candidate parameter vector, which is fed to the Metric Calculator module. The Metric Calculator module evaluates the candidate parameter vector, using a metric based on the residual of the actual and the predicted commands. The predicted commands are calculated utilizing the candidate parameter vector and the vehicle state vector, which is available via a complete navigation module. Then, the metric is directly fed back to the Optimization Algorithm module, and it is used to correct the estimated parameter vector. The procedure continues iteratively until the convergence properties are met. The proposed method is generic, demonstrates quick convergence and does not require a linear formulation of the model with respect to the parameter vector. The applicability and performance of the proposed algorithm is experimentally verified using the AUV Girona 500. © 2013 IEEE

ICAR: endoscopic skull‐base surgery

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Hypovitaminosis D is Independently Associated with Metabolic Syndrome in Obese Patients

BACKGROUND: Metabolic syndrome (MS) and hypovitaminosis D represent two of the most diffuse condition worldwide, reaching pandemic proportions in industrialized countries, and are both strongly associated with obesity. This study set out to evaluate the presence of an independent association between hypovitaminosis D and MS in an adult population of obese subjects with/without MS. METHODS: We recruited 107 consecutive obese subjects, 61 with MS (age(mean±SD) 45.3±13.3 years, BMI(mean±SD): 43.1±8.3 kg/m(2)) and 46 without MS (age: 41.8±11.5, p = n.s., BMI:41.6±6.5 kg/m(2), p = n.s.) comparable for sex, BMI, waist circumference and body fat mass, evaluated by bioimpedentiometry. 25(OH) vitamin D(3) levels were measured by colorimetric method. Insulin resistance was estimated by fasting blood insulin, HOMA-IR and ISI. RESULTS: Serum 25(OH)D(3) levels were significantly lower in MS obese patients than in obese subjects without MS (median(range) 13.5(3.3–32) vs 17.4(5.1–37.4), p<0.007). Low 25(OH)D(3) levels correlated with glycaemia (p<0.007), phosphate (p<0.03), PTH (p<0.003) and the MS (p<0.001). Multivariate model confirmed that low 25(OH)D(3) levels were associated with the diagnosis of MS in obese patients independently from gender, age, serum PTH and body fat mass. After stratifying the study population according to 25(OH)D(3) concentrations, patients in the lowest quartile showed a markedly increased prevalence of MS compared to those in the highest quartile (OR = 4.1, CI 1.2–13.7, p = 0.02). CONCLUSIONS: A powerful association exists between hypovitaminosis D and MS in obese patients independently from body fat mass and its clinical correlates. This indicates that the association between low 25(OH) D(3) levels and MS is not merely induced by vitamin D deposition in fat tissue and reinforces the hypothesis that hypovitaminosis D represent a crucial independent determinant of MS

TRF2 inhibits a cell-extrinsic pathway through which natural killer cells eliminate cancer cells

Dysfunctional telomeres suppress tumour progression by activating cell-intrinsic programs that lead to growth arrest. Increased levels of TRF2, a key factor in telomere protection, are observed in various human malignancies and contribute to oncogenesis. We demonstrate here that a high level of TRF2 in tumour cells decreased their ability to recruit and activate natural killer (NK) cells. Conversely, a reduced dose of TRF2 enabled tumour cells to be more easily eliminated by NK cells. Consistent with these results, a progressive upregulation of TRF2 correlated with decreased NK cell density during the early development of human colon cancer. By screening for TRF2-bound genes, we found that HS3ST4--a gene encoding for the heparan sulphate (glucosamine) 3-O-sulphotransferase 4--was regulated by TRF2 and inhibited the recruitment of NK cells in an epistatic relationship with TRF2. Overall, these results reveal a TRF2-dependent pathway that is tumour-cell extrinsic and regulates NK cell immunity