Wavelet maxima curves of surface latent heat flux associated with two recent Greek earthquakes

International audienceMulti sensor data available through remote sensing satellites provide information about changes in the state of the oceans, land and atmosphere. Recent studies have shown anomalous changes in oceans, land, atmospheric and ionospheric parameters prior to earthquakes events. This paper introduces an innovative data mining technique to identify precursory signals associated with earthquakes. The proposed methodology is a multi strategy approach which employs one dimensional wavelet transformations to identify singularities in the data, and an analysis of the continuity of the wavelet maxima in time and space to identify the singularities associated with earthquakes. The proposed methodology has been employed using Surface Latent Heat Flux (SLHF) data to study the earthquakes which occurred on 14 August 2003 and on 1 March 2004 in Greece. A single prominent SLHF anomaly has been found about two weeks prior to each of the earthquakes

Recurrent herpes simplex virus-1 infection induces hallmarks of neurodegeneration and cognitive deficits in mice

Herpes simplex virus type 1 (HSV-1) is a DNA neurotropic virus, usually establishing latent infections in the trigeminal ganglia followed by periodic reactivations. Although numerous findings suggested potential links between HSV-1 and Alzheimer's disease (AD), a causal relation has not been demonstrated yet. Hence, we set up a model of recurrent HSV-1 infection in mice undergoing repeated cycles of viral reactivation. By virological and molecular analyses we found: i) HSV-1 spreading and replication in different brain regions after thermal stress-induced virus reactivations; ii) accumulation of AD hallmarks including amyloid-\u3b2 protein, tau hyperphosphorylation, and neuroinflammation markers (astrogliosis, IL-1\u3b2 and IL-6). Remarkably, the progressive accumulation of AD molecular biomarkers in neocortex and hippocampus of HSV-1 infected mice, triggered by repeated virus reactivations, correlated with increasing cognitive deficits becoming irreversible after seven cycles of reactivation. Collectively, our findings provide evidence that mild and recurrent HSV-1 infections in the central nervous system produce an AD-like phenotype and suggest that they are a risk factor for AD

Herpes Simplex Virus-1 in the Brain: The Dark Side of a Sneaky Infection

Herpes simplex virus-1 (HSV-1) establishes latency preferentially in sensory neurons of peripheral ganglia. A variety of stresses can induce recurrent reactivations of the virus, which spreads and then actively replicates to the site of primary infection (usually the lips or eyes). Viral particles produced following reactivation can also reach the brain, causing a rare but severe form of diffuse acute infection, namely herpes simplex encephalitis. Most of the time, this infection is clinically asymptomatic. However, it was recently correlated with the production and accumulation of neuropathological biomarkers of Alzheimer's disease. In this review we discuss the different cellular and molecular mechanisms underlying the acute and long-term damage caused by HSV-1 infection in the brain

Herpes simplex virus type 1 (hsv-1) infection as a risk factor for ad: possible role of neuroinflammation and oxidative stress

Background: Several evidence suggest HSV-1 as a potential risk factors for Alzheimer’s disease (AD). Objective: Herein we design in vitro and in vivo study to evaluate whether HSV-1 primary infection, in glia/neuron cultures, and repeated HSV-1 reactivations, in mice, may concur to accumulation of the main AD hallmarks, as b-amyloid peptides (Aβs) and neurofibrillary tangles, mainly composed by hyperphosphorylated tau. We also evaluated the potential role of HSV-1 in inducing oxidative stress and neuroinflammation, in terms of cytokines production and gliosis. Patients and Methods / Material and Methods: HSV-1 infected BALB/c mice were subjected to multiple virus reactivations. Virus replication in the brain was analyzed through PCR and RT-PCR. AD and oxidative stress hallmarks were analyzed by multiplex, immunofluorescence, western blotting and fluorymetry Results: We found that HSV-1, 4h after infection, induces in glial/neuronal cells a significant increase in the level of ROS and HNE, a marker of lipid peroxidation. This timing is consistent with our previous data showing the activation of redox-regulated pathway inducing Aβs production. Following HSV-1 multiple reactivations, we found in mouse brains: 1) viral TK and ICP4 genes in cortex and hippocampal tissues, indicating that HSV-1 is able to reach and replicate in those brain regions mostly affected during AD; 2) increased levels of HNE, protein nytrosylation (3-NT), and carbonylation; 3) enhanced levels of IL-6, IL-1b cytokines and gliosis; 4) accumulation of Aβs and altered tau phosphorylation. Conclusion: Altogether these data support the hypothesis that repeated HSV-1 infections may contribute to the neurodegeneration typical of AD and suggest a potential pathogenic role for virus-induced oxidative stress and neuroinflammation

Stimulation of the serotonin receptor 7 restores brain histone H3 acetylation and MeCP2 corepressor protein levels in a female mouse model of Rett syndrome

Rett syndrome (RTT) is a rare neurological disorder caused by mutations in the X-linked MECP2 gene, characterized by severe behavioral and physiological impairments for which no cure is available. The stimulation of serotonin receptor 7 (5-HT7R) with its selective agonist LP-211 (0.25 mg/kg/day for 7 days) was proved to rescue neurobehavioral alterations in a mouse model of RTT. In the present study, we aimed at gaining insight into the mechanisms underpinning the efficacy of 5-HT7R pharmacological stimulation by investigating its epigenetic outcomes in the brain of RTT female mice bearing a truncating MeCP2 mutation. Treatment with LP-211 normalized the reduced histone H3 acetylation and HDAC3/NCoR levels, and increased HDAC1/Sin3a expression in RTT mouse cortex. Repeated 5-HT7R stimulation also appeared to strengthen the association between NCoR and MeCP2 in the same brain region. A different profile was found in RTT hippocampus, where LP-211 rescued H3 hyperacetylation and increased HDAC3 levels. Overall, the present data highlight a new scenario on the relationship between histone acetylation and serotoninergic pathways. 5-HT7R is confirmed as a pivotal therapeutic target for the recovery of neuronal function supporting the translational value of this promising pharmacological approach for RTT

Synthesis and preliminary pharmacological evaluation of 5-hydroxy-and 5,6-dihydroxy-1,2,3,7,12,12a-hexahydrobenzo [5,6]cycloheptal [1,2,3-ij]isoquinoline derivatives as dopamine receptor ligands

A series of 5-hydroxy- and 5,6-dihydroxy- 1,2,3,7,12,12a-hexahydrobenzo[5,6]cyclohepta[1,2,3-iJ]isoquinoline derivatives (5a-e and 6a-e) were synthesized as conformationally rigid analogues of 1-benzyltetrahydroisoquinoline and evaluated for their affinity at D-1 and D-2 dopamine receptors. All compounds showed lower D1 and D affinities than dopamine. The 5-hydroxy-1-methyl-2,3,12,12a-hexahydrobenzo[5,6]cyclohepta[1,2,3-ij] 5a and the 5,6dihydroxy analogue 6a showed D-2 agonist activity. This was proved by their effects on prolactin release from primary cultures of rat anterior pituitary cells. Molecular modeling studies showed that the geometric parameters (namely the distances from meta and para hydroxyl oxygens to the nitrogen and the height of nitrogen from the hydroxylated phenyl ring plane) of the dopaminergic pharmacophore embedded in our compounds have lower values in comparison with those observed in D-1 and D-2 selective ligands. (C) 2001 Elsevier Science Ltd. All rights reserved