Motion Estimation and Compensation in Automotive MIMO SAR

With the advent of self-driving vehicles, autonomous driving systems will have to rely on a vast number of heterogeneous sensors to perform dynamic perception of the surrounding environment. Synthetic Aperture Radar (SAR) systems increase the resolution of conventional mass-market radars by exploiting the vehicle's ego-motion, requiring a very accurate knowledge of the trajectory, usually not compatible with automotive-grade navigation systems. In this regard, this paper deals with the analysis, estimation and compensation of trajectory estimation errors in automotive SAR systems, proposing a complete residual motion estimation and compensation workflow. We start by defining the geometry of the acquisition and the basic processing steps of Multiple-Input Multiple-Output (MIMO) SAR systems. Then, we analytically derive the effects of typical motion errors in automotive SAR imaging. Based on the derived models, the procedure is detailed, outlining the guidelines for its practical implementation. We show the effectiveness of the proposed technique by means of experimental data gathered by a 77 GHz radar mounted in a forward looking configuration.Comment: 14 page

A possible role for nitric oxide in modulating the functional cyclosporine toxicity by arginine

A possible role for nitric oxide in modulating the functional cyclosporine toxicity by arginine. The renal damage consequent to cyclosporine A (CsA) administration ranges from hemodynamic alterations to irreversible chronic lesions. The initial vasoconstriction depends upon the imbalance between the various modulators of the renal vascular tone, among which the most powerful are endothelins and nitric oxide (NO). CsA could play a crucial role by inhibiting the Ca++/calmodulin-mediated activation of the constitutive NO synthase (NOS) isoform, which converts L-arginine (L-Arg) into NO and citrulline, with a 1:1 stoichiometry. To investigate the possibility of modulating CsA nephrotoxicity with L-Arg we studied six groups (G) of Lewis rats treated with daily gavage up to eight weeks: G1, CsA 40 mg/kg; G2, G1 plus L-Arg 300 mg/kg; G3, G2 plus the competitive inhibitor of NOS, NG-nitro-L-Arg (L-NNA); G4, L-Arg alone; G5, L-NNA alone; and G6, controls receiving vehicle alone. After eight weeks L-Arg treated rats were protected against the toxic effects of CsA [creatinine (Cr) values, G2, 0.62 ± 0.05 mg/dl vs. G1, 0.99 ± 0.16 mg/dl, P < 0.001; proteinuria (P), G2, 7.2 ± 1.02 mg/day vs. G1, 15.1 ± 1.9 mg/day, P < 0.01]. The administration of L-NNA abolished the protective effect of L-Arg (G3, Cr 1.23 ± 0.16 mg/dl; P 16.9 = 2.3; P < 0.02 and P < 0.005, respectively vs. G2). The levels of Cr in G2 rats were superimposable to control groups. The NOS activity, evaluated by measuring [3H]citrulline formation from [3H]L-Arg in kidney homogenates, was blocked by L-NNA in G5 (0.019 ± 0.009 pmol/min/mg proteins vs. G6 0.047 ± 0.002, P < 0.01). NOS activity was significantly increased versus controls in G1 (0.110 ± 0.032, P < 0.01) and G2 (0.088 ± 0.009, P < 0.02), while L-NNA reversed this phenomenon (G3, 0.052 ± 0.03). The expression of mRNA encoding for cNOS and iNOS was only slightly increased in CsA-treated rats. We suggest that CsA treatment increases NOS activity in the kidney by a mechanism which does not require a de novo synthesis of the enzyme. Such an increase, that may be devoted to counterbalance the vasoconstrictive effects of the drug, is unable to reduce the toxic effect of CsA in the absence of exogenous L-Arg. Administration of L-Arg is likely to reduce CsA nephrotoxicity by accomplishing the higher request of activated NOS for its substrate, thus potentiating NO synthesis in the kidney.

Epidemiological patterns of asbestos exposure and spatial clusters of incident cases of malignant mesothelioma from the Italian national registry

Abstract BACKGROUND: Previous ecological spatial studies of malignant mesothelioma cases, mostly based on mortality data, lack reliable data on individual exposure to asbestos, thus failing to assess the contribution of different occupational and environmental sources in the determination of risk excess in specific areas. This study aims to identify territorial clusters of malignant mesothelioma through a Bayesian spatial analysis and to characterize them by the integrated use of asbestos exposure information retrieved from the Italian national mesothelioma registry (ReNaM). METHODS: In the period 1993 to 2008, 15,322 incident cases of all-site malignant mesothelioma were recorded and 11,852 occupational, residential and familial histories were obtained by individual interviews. Observed cases were assigned to the municipality of residence at the time of diagnosis and compared to those expected based on the age-specific rates of the respective geographical area. A spatial cluster analysis was performed for each area applying a Bayesian hierarchical model. Information about modalities and economic sectors of asbestos exposure was analyzed for each cluster. RESULTS: Thirty-two clusters of malignant mesothelioma were identified and characterized using the exposure data. Asbestos cement manufacturing industries and shipbuilding and repair facilities represented the main sources of asbestos exposure, but a major contribution to asbestos exposure was also provided by sectors with no direct use of asbestos, such as non-asbestos textile industries, metal engineering and construction. A high proportion of cases with environmental exposure was found in clusters where asbestos cement plants were located or a natural source of asbestos (or asbestos-like) fibers was identifiable. Differences in type and sources of exposure can also explain the varying percentage of cases occurring in women among clusters. CONCLUSIONS: Our study demonstrates shared exposure patterns in territorial clusters of malignant mesothelioma due to single or multiple industrial sources, with major implications for public health policies, health surveillance, compensation procedures and site remediation programs