Giovanni Corsini

A tutorial overview of anomaly detection in hyperspectral images

In this paper, a tutorial overview on anomaly detection for hyperspectral electro-optical systems is presented. This tutorial is focused on those techniques that aim to detect small man-made anomalies typically found in defense and surveillance applications. Since a variety of methods have been proposed for detecting such targets, this tutorial places emphasis on the techniques that are either mathematically more tractable or easier to interpret physically. These methods are not only more suitable for a tutorial publication, but also an essential to a study of anomaly detection. Previous surveys on this subject have focused mainly on anomaly detectors developed in a statistical framework and have been based on well-known background statistical models. However, the most recent research trends seem to move away from the statistical framework and to focus more on deterministic and geometric concepts. This work also takes into consideration these latest trends, providing a wide theoretical review without disregarding practical recommendations about algorithm implementation. The main open research topics are addressed as well, the foremost being algorithm optimization, which is required for embodying anomaly detectors in real-time systems.

Nicotine prevents experimental Parkinsonism in rodents and induces striatal increase of neurotrophic factors

Abstract: The repeated finding of an apparent protective effect of cigarette smoking on the risk of Parkinsons disease is one of the few consistent results in the epidemiology of this disorder. Among the numerous substances that originate from tobacco smoke, nicotine is by far the most widely studied. Nicotine is a natural alkaloid that has considerable stimulatory effects on the CNS. Its effects on the CNS are mediated by the activation of neuronal heteromeric acetylcholine‐gated ion channel receptors (nAChRs, also termed nicotinic acetylcholine receptors). In the present study, we describe the neuroprotective effects of (−)‐nicotine in two animal models of parkinsonism: diethyldithiocarbamate‐induced enhancement of 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine toxicity in mice and methamphetamine‐induced neurotoxicity in rats and mice. The neuroprotective effect of (−)‐nicotine was very similar to that of the noncompetitive NMDA receptor antagonist (+)‐MK‐801. In parallel experiments, we found that (−)‐nicotine induces the basic fibroblast growth factor‐2 (FGF‐2) and the brain‐derived neurotrophic factor in rat striatum. The effect of (−)‐nicotine on the induction of FGF‐2 was prevented by the nAChR antagonist mecamylamine. We also found that (+)‐MK‐801 was able to induce FGF‐2 in the striatum. As trophic factors have been reported to be neuroprotective for dopaminergic cells, our data suggest that the increase in neurotrophic factors is a possible mechanism by which (−)‐nicotine protects from experimental parkinsonisms.

MK-801 Prevents 1-Methyl-4-Phenyl-1,2,3,6-Tetrahydropyridine-Induced Parkinsonism in Primates

Abstract: In cynomologus monkeys, systemic administration of MK‐801, a noncompetitive antagonist for the N‐methyl‐4‐aspartate receptor, prevented the development of the parkinsonian syndrome induced by the neurotoxin 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine (MPTP). MK‐801 also attenuated dopamine depletion in the caudate and putamen and protected dopaminergic neurons in the substantia nigra from the degeneration induced by the neurotoxin. Nevertheless, 7 days after MPTP administration in the caudate and putamen of monkeys also receiving MK‐801, the levels of toxic l‐methyl‐4‐phenylpyridinium were even higher than those measured in monkeys receiving MPTP alone. This indicates that the protective action of MK‐801 is not related to MPTP metabolism and strongly suggests that, in primates, the excitatory amino acids could play a crucial role in the mechanism of the selective neuronal death induced by MPTP.

Signal-Dependent Noise Modeling and Model Parameter Estimation in Hyperspectral Images

In this paper, a novel method to characterize random noise sources in hyperspectral (HS) images is proposed. Noise is described using a parametric model that accounts for the dependence of noise variance on the useful signal. Such model takes into account the photon noise contribution and is therefore suitable for noise characterization in the data acquired by new-generation HS sensors where electronic noise is not dominant. A new algorithm is developed for the estimation of noise parameters which consists of two steps. First, the noise and signal realizations are extracted from the original image by resorting to the multiple-linear-regression-based approach. Then, the model parameters are estimated by using a maximum likelihood approach. The new method does not require the intervention of a human operator and the selection of homogeneous regions in the scene. The performance of the new technique is analyzed on simulated HS data. Results on real data are also presented and discussed. Images acquired with a new-generation HS camera are analyzed to give an experimental evidence of the dependence of random noise on the signal level and to show the results of the estimation algorithm. The algorithm is also applied to a well-known Airborne Visible/Infrared Imaging Spectrometer data set in order to show its effectiveness when noise is dominated by the signal-independent term.

Functional Role of the Third Cytoplasmic Loop in Muscarinic Receptor Dimerization

By means of the expression of two chimeric receptors, α2/m3 and m3/α2, in which the carboxyl-terminal receptor portions, containing transmembrane (TM) domains VI and VII, were exchanged between the α2C adrenergic and the m3 muscarinic receptor, Maggio et al. (Maggio, R., Vogel, Z., and Wess, J. (1993) Proc. Natl. Acad. Sci. U. S. A. 90, 3103-31073) demonstrated that G protein-linked receptors are able to interact functionally with each other at the molecular level to form (hetero)dimers. In the present study we tested the hypothesis that interaction between receptors might depend on the presence of a long third intracellular (i3) loop and that shortening this loop could impair the capability of receptors to form dimers. To address this question, we initially created short chimeric α2 adrenergic/m3 muscarinic receptors in which 196 amino acids were deleted from the i3 loop (α2/m3-short and m3/α2-short). Although co-transfection of α2/m3 and m3/α2 resulted in the appearance of specific binding, the co-expression of the two short constructs (α2/m3-short and m3/α2-short), either together or in combination, respectively, with m3/α2 and α2/m3 did not result in any detectable binding activity. In another set of experiments, a mutant m3 receptor, m3/m2(16aa), containing 16 amino acids of the m2 receptor sequence at the amino terminus of the third cytoplasmic loop, which was capable of binding muscarinic ligands but was virtually unable to stimulate phosphatidylinositol hydrolysis, was also mutated in the i3 loop, resulting in the m3/m2(16aa)-short receptor. Although co-transfection of m3/m2(16aa) with a truncated form of the m3 receptor (m3-trunc, containing an in frame stop codon after amino acid codon 272 of the rat m3 sequence) resulted in a considerable carbachol-stimulated phosphatidylinositol breakdown, the co-transfection of m3/m2(16aa)-short with the truncated form of the m3 receptor did not result in any recovery of the functional activity. Thus, these data suggest that intermolecular interaction between muscarinic receptors, involving the exchange of amino-terminal (containing TM domains I-V) and carboxyl-terminal (containing TM domains VI and VII) receptor fragments depends on the presence of a long i3 loop. One may speculate that when alternative forms of receptors with a different length of the i3 loop exist, they could have a different propensity to dimerize.

Retrieval of sea water optically active parameters from hyperspectral data by means of generalized radial basis function neural networks

The authors present a new methodology for estimating the concentration of sea water optically active constituents from remotely sensed hyperspectral data, based on generalized radial basis function neural networks (GRBF-NNs). This family of NNs is particularly suited to approximate relationships like those between hyperspectral reflectance data and the concentrations of optically active constituents of the water body, which are highly nonlinear, especially in case II waters. Three main water constituents are taken into account: phytoplankton, nonchlorophyllous particles, and yellow substance. Each parameter is estimated by means of a specific multi-input single-output GRBF-NN. The authors adopt a recently proposed network learning strategy based on the combined use of the regression tree procedure and forward selection. The effectiveness of this approach, which is completely general and can be easily applied to any hyperspectral sensor, is proved using data simulated with an ocean color model over the channels of the medium resolution imaging spectrometer (MERIS), the new generation ESA sensor to be launched in 2001. The authors define the estimation algorithms over waters of cases I, II, and I+II and compare their performance with that of classical band-ratio, single-band, and multilinear algorithms. Generally, the GRBF-NN algorithms outperform the classical ones, except for the multilinear over case I waters. A particular improvement Is over case II waters, where the mean square error (MSE) can be reduced by one or two orders of magnitude over the error of multilinear and band-ratio algorithms, respectively.

Striatal increase of neurotrophic factors as a mechanism of nicotine protection in experimental parkinsonism.

SummaryThe repeated finding of an apparent protective effect of cigarette smoking on the risk of Parkinsons disease is one of the few consistent results in the epidemiology of this disorder. Among the innumerous substances that originate from tobacco smoke, nicotine is by far the most widely studied, and the most likely candidate for a protective effect against neuronal degeneration in Parkinsons disease. Nicotine is a natural alkaloid that has considerable stimulatory effects on the central nervous system (CNS). Its effects on the CNS are mediated by the activation of neuronal heteromeric acetylcholine-gated ion channel receptors (nAChR, also termed nicotinic acetylcholine receptors). In the present study, we describe the neuroprotective effects of (−)nicotine in two animal models of parkinsonism: the diethyldithiocarbamate (DDC)-induced enhancement of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) toxicity in mice, and the methamphetamine-induced neurotoxicity in rats and mice. In parallel experiments, we found that (−)nicotine induces the basic fibroblast growth factor (FGF-2) and the brain-derived neurotrophic factor (BDNF) in rat striatum. As FGF-2 and BDNF have been reported to be neuroprotective for dopaminergic cells, our data indicate that the increase in neurotrophic factors is a possible mechanism by which (−)nicotine protects from experimental parkinsonisms. Moreover, they suggest that nAChR agonists could be of potential benefit in the progression of Parkinsons disease.

The impact of G‐protein‐coupled receptor hetero‐oligomerization on function and pharmacology

Although highly controversial just a few years ago, the idea that G‐protein‐coupled receptors (GPCRs) may undergo homo‐oligomerization or hetero‐oligomerization has recently gained considerable attention. The recognition that GPCRs may exhibit either dimeric or oligomeric structures is based on a number of different biochemical and biophysical approaches. Although much effort has been spent to demonstrate the mechanism(s) by which GPCRs interact with each other, the physiological relevance of this phenomenon remains elusive. An additional source of uncertainty stems from the realization that homo‐oligomerization and hetero‐oligomerization of GPCRs may affect receptor binding and activity in different ways, depending on the type of interacting receptors. In this brief review, the functional and pharmacological effects of the hetero‐oligomerization of GPCR on binding and cell signaling are critically analyzed.

Inhibition of nitric oxide synthase dramatically potentiates seizures induced by kainic acid and pilocarpine in rats

We investigated whether the severity of convulsions evoked by kainic acid and pilocarpine is modified in nitric oxide synthase inhibitor-treated rats. We found that chronic treatment (4 days) with NW-nitro-L-arginine greatly potentiates seizures induced by both convulsants suggesting a potential role for nitric oxide in mechanisms regulating seizure induction and propagation.

Potent activation of dopamine D3/D2 heterodimers by the antiparkinsonian agents, S32504, pramipexole and ropinirole

Recombinant, human dopamine D3 and D2 receptors form functional heterodimers upon co‐expression in COS‐7 cells. Herein, actions of the antiparkinsonian agents, S32504, ropinirole and pramipexole, at D3/D2L heterodimers were compared to their effects at the respective monomers and at split, chimeric D3trunk/D2tail and D2trunk/D3tail receptors: the trunk incorporated transmembrane domains (TDs) I–V and the tail TDs VI and VII. In binding assays with the antagonist [3H]nemonapride, all agonists were potent ligands of D3 receptors showing, respectively, 100‐, 18‐ and 56‐fold lower affinity at D2L receptors, mimicking the selective D3 receptor antagonist, S33084 (100‐fold). At D3trunk/D2tail receptors, except for ropinirole, all drugs showed lower affinities than at D3 sites, whereas for D2trunk/D3tail receptors, affinities of all drugs were higher than at D2L sites. The proportion of high affinity binding sites recognized by S32504, pramipexole and ropinirole in membranes derived from cells co‐expressing D3 and D2L sites was higher than in an equivalent mixture of membranes from cells expressing D3 or D2L sites, consistent with the promotion of heterodimer formation. In contrast, the percentage of high and low affinity sites (biphasic isotherms) recognized by S33084 was identical. Functional actions were determined by co‐transfection of a chimeric adenylyl cyclase (AC)‐V/VI insensitive to D3 receptors. Accordingly, D3 receptor‐transfected cells were irresponsive whereas, in D2L receptor‐transfected cells, agonists suppressed forskolin‐stimulated cAMP production with modest potencies. In cells co‐transfected with D3 and D2L receptors, S32504, ropinirole and pramipexole potently suppressed AC‐V/VI with EC50s 33‐, 19‐ and 11‐fold lower than at D2L receptors, respectively. S32504 also suppressed AC‐V/VI activity at split D3trunk/D2tail and D2trunk/D3tail chimeras transfected into COS‐7 cells. In conclusion, antiparkinson agents behave as potent agonists at D3/D2‘heterodimers’, though any role in their actions in vivo remains to be demonstrated.