Statistical real-time model for performance prediction of ship detection from microsatellite electro-optical imagers

For locating maritime vessels longer than 45 meters, such vessels are required to set up an Automatic Identification System (AIS) used by vessel traffic services. However, when a boat is shutting down its AIS, there are no means to detect it in open sea. In this paper, we use Electro-Optical (EO) imagers for noncooperative vessel detection when the AIS is not operational. As compared to radar sensors, EO sensors have lower cost, lower payload, and better computational processing load. EO sensors are mounted on LEO microsatellites. We propose a real-time statistical methodology to estimate sensor Receiver Operating Characteristic (ROC) curves. It does not require the computation of the entire image received at the sensor. We then illustrate the use of this methodology to design a simple simulator that can help sensor manufacturers in optimizing the design of EO sensors for maritime applications

Age-Related Impairment of Ultrasonic Vocalization in Tau.P301L Mice: Possible Implication for Progressive Language Disorders

Tauopathies, including Alzheimer's Disease, are the most frequent neurodegenerative diseases in elderly people and cause various cognitive, behavioural and motor defects, but also progressive language disorders. For communication and social interactions, mice produce ultrasonic vocalization (USV) via expiratory airflow through the larynx. We examined USV of Tau.P301L mice, a mouse model for tauopathy expressing human mutant tau protein and developing cognitive, motor and upper airway defects.At age 4-5 months, Tau.P301L mice had normal USV, normal expiratory airflow and no brainstem tauopathy. At age 8-10 months, Tau.P301L mice presented impaired USV, reduced expiratory airflow and severe tauopathy in the periaqueductal gray, Kolliker-Fuse and retroambiguus nuclei. Tauopathy in these nuclei that control upper airway function and vocalization correlates well with the USV impairment of old Tau.P301L mice.In a mouse model for tauopathy, we report for the first time an age-related impairment of USV that correlates with tauopathy in midbrain and brainstem areas controlling vocalization. The vocalization disorder of old Tau.P301L mice could be, at least in part, reminiscent of language disorders of elderly suffering tauopathy

Early structural and functional defects in synapses and myelinated axons in stratum lacunosum moleculare in two preclinical models for tauopaty

The stratum lacunosum moleculare (SLM) is the connection hub between entorhinal cortex and hippocampus, two brain regions that are most vulnerable in Alzheimer’s disease. We recently identified a specific synaptic deficit of Nectin-3 in transgenic models for tauopathy. Here we defined cognitive impairment and electrophysiological problems in the SLM of Tau.P301L mice, which corroborated the structural defects in synapses and dendritic spines. Reduced diffusion of DiI from the ERC to the hippocampus indicated defective myelinated axonal pathways. Ultrastructurally, myelinated axons in the temporoammonic pathway (TA) that connects ERC to CA1 were damaged in Tau.P301L mice at young age. Unexpectedly, the myelin defects were even more severe in bigenic biGT mice that co-express GSK3β with Tau.P301L in neurons. Combined, our data demonstrate that neuronal expression of protein Tau profoundly affected the functional and structural organization of the entorhinal-hippocampal complex, in particular synapses and myelinated axons in the SLM. White matter pathology deserves further attention in patients suffering from tauopathy and Alzheimer’s disease

beta-site amyloid precursor protein cleaving enzyme 1 increases amyloid deposition in brain parenchyma but reduces cerebrovascular amyloid angiopathy in aging BACE x APP[V7171] double-transgenic mice

The generation of amyloid peptides (Aß) from the amyloid precursor protein (APP) is initiated by ß-secretase (BACE), whereas subsequent {gamma}-secretase cleavage mediated by presenilin-1, produces Aß peptides mainly of 40 or 42 amino acids long. In addition, alternative ß'-cleavage of APP at position 11 of the amyloid sequence results in N-truncated Aß(11-40/42) peptides, but the functional significance or pathological impact is unknown. Here we demonstrate that in the brain of BACE x APP[V717I] double-transgenic mice, amyloidogenic processing at both Asp1 and Glu11 is increased resulting in more and different Aß species and APP C-terminal fragments. Pathologically, BACE significantly increased the number of diffuse and senile amyloid plaques in old double-transgenic mice. Unexpectedly, vascular amyloid deposition was dramatically lower in the same BACE x APP[V717I] double-transgenic mice, relative to sex- and age-matched APP[V717I] single-transgenic mice in the same genetic background. The tight inverse relation of vascular amyloid to the levels of the less soluble N-terminally truncated Aß peptides is consistent with the hypothesis that vascular amyloid deposition depends on drainage of excess tissue Aß. This provides biochemical evidence in vivo for the preferential contribution of N-truncated Aß to parenchymal amyloid deposition in contrast to vascular amyloid pathology