On the benefits of self-taught learning for brain decoding.

Context: We study the benefits of using a large public neuroimaging database composed of functional magnetic resonance imaging (fMRI) statistic maps, in a self-taught learning framework, for improving brain decoding on new tasks. First, we leverage the NeuroVault database to train, on a selection of relevant statistic maps, a convolutional autoencoder to reconstruct these maps. Then, we use this trained encoder to initialize a supervised convolutional neural network to classify tasks or cognitive processes of unseen statistic maps from large collections of the NeuroVault database.

SAPHIR: a Shiny application to analyze tissue section images.

Study of cell populations in tissues using immunofluorescence is a powerful method for both basic and medical research. Image acquisitions performed by confocal microscopy notably allow excellent lateral resolution and more than 10 parameter measurements when using spectral or multiplex imaging. Analysis of such complex images can be very challenging and easily lead to bias and misinterpretation.

Clinical Psychology and Cardiovascular Disease: An Up-to-Date Clinical Practice Review for Assessment and Treatment of Anxiety and Depression.

The aim of the present review is underline the association between cardiac diseases and anxiety and depression. In the first part of the article, there is a description of anxiety and depression from the definitions of DSM-IV TR. In the second part, the authors present the available tests and questionnaires to assess depression and anxiety in patients with cardiovascular disease.

Glycosaminoglycans co-administration enhance insulin-like growth factor-I neuroprotective and neuroregenerative activity in traumatic and genetic models of motor neuron disease: a review.

In this report it is shown how glycosaminoglycans and insulin-like growth factor-I (IGF-I) promote muscle reinnervation and prevent motor neuron death in experimental models of motor neuron disease. Such effect appears to be mediated by insulin-like growth factor-1. The glycosaminoglycan moiety of proteoglycans is a constituent of the basal lamina active on nerve regeneration by means of the interaction with laminin and with several growth factors.

Long-term neuroprotective effects of glycosaminoglycans-IGF-I cotreatment in the motor neuron degeneration (mnd) mutant mouse.

This study shows that cotreatment with insulin-like growth factor-I (IGF-I) and glycosaminoglycans (GAGs) prevents the onset of neuromuscular deficit in the m/m mutant mouse. These mice show a mid-to-late-life onset of progressive paralysis of the hind limb, that is correlated with altered innervation and reduced nerve-evoked isometric twitch tension in the extensor digitorum longus (EDL) muscle. Almost 50% of EDL nerve endings are negative for antisynaptophysin staining, while retrograde labelling with beta-cholera-toxin coupled to type IV horseradish and quantitative histological analysis show a small loss of EDL and lumbar cord motor neurons.

Perinatal supplementation of low doses of ethanol enhances 5-HT restoration in the central nervous system.

It has been reported that long-term administration of ethanol has deleterious effects on the central nervous system; the alterations are particularly evident if the exposure occurs during development. Our study shows that rat perinatal administration of 3% and 6% ethanol does not alter development of serotonin (5-HT) pathways in the central nervous system, while their reactive changes triggered by neonatal lesioning are greatly altered. The administration of 5, 7-dihydroxytriptamine (5,7-DHT) within 6 hours from birth causes 5-HT fiber degeneration throughout the central nervous system.

Inhibition of high glucose-induced protein mono-ADP-ribosylation restores neuritogenesis and sodium-pump activity in SY5Y neuroblastoma cells.

The exposure of SY5Y neuroblastoma cells to high concentrations of glucose, fructose, or galactose is an experimental model commonly used for in vitro evaluation of typical neuronal alterations observed in diabetes mellitus. In the present study, we observed that 2 weeks of exposure to high carbohydrate concentrations caused both a significant impairment in neurite formation induced by supplementation of retinoic acid or by subtraction of fetal calf serum to the culture medium and a marked reduction in Na(+)-K(+)-ATPase activity. However, only the exposure to high millimoles of glucose caused an enhancement of mono-ADP-ribosylation, typical of diabetes mellitus, affecting at least five proteins.

Progressive and selective changes in neurotrophic factor expression and substance p axonal transport induced by perinatal diabetes: protective action of antioxidant treatment.

Diabetes-induced embryo malformations and growth retardation are correlated with a variety of biochemical changes including oxidative stress. In this study, we show that the morphological alterations are correlated with progressive and selective changes of mRNA expression in specific neurotrophic factors. At embryological stage E-17, diabetes affected both embryo growth and NGF mRNA expression, which was reduced by as much as 90 and 56% in target tissues of sensory system such as tongue and intestine, respectively.

[Kinetics of sialylation of Neisseria gonorrhoeae by radiolabelled cytidine 5'monophospho-N-acetyl neuraminic acid].

Neisseria gonorrhoeae (Strain A) induces a sialyl-transferase when treated with a very low concentration of cytidine 5'monophospho-N-acetyl neuraminic acid, 2 x 10(-3) nmol.ml-1, a concentration which is insufficient to produce an adequate resistance to human serum complement. The sialyl-transferase activity was detected by measurement of fixed 14C radio-labeled sialyl groups.

Perinatal morphine II: changes in cortical plasticity.

We have previously shown that perinatal exposure to morphine impairs reactive plasticity of serotonin (5-HT) neurons following selective neonatal lesion (Gorio et al., J Neurosci Res 34:462-471, 1993). This study shows that morphine inhibits also that the compensatory sprouting of intact axons after partial denervation.

Expression of endothelin and ETB receptors in the megakaryoblastic MEG-01 cell line.

The presence of endothelin (ET) receptors and the nature of the subtype and expression of ET were investigated in the human megakaryoblastic cell line MEG-01. By the RT-PCR procedure, we have shown that both ETA and ETB receptor subtype mRNAs are expressed in the cells. However, binding experiments have shown that the selective ETB receptor antagonist BQ788, but not the selective ETA receptor antagonist BQ123, competes with the specific binding of [125I]ET-1.

Perinatal morphine treatment inhibits pruning effect and regeneration of serotoninergic pathways following neonatal 5,7-HT lesions.

Lesion of the serotoninergic system in neonate rats is an ideal model for assessing the activity of chemical substances capable of affecting neuronal plasticity and regeneration (Jonsson et al., Dev Brain Res 16: 171-180, 1984). Treatment of newborn rats within 6 hr from birth with the selective neurotoxin 5,7-dihydroxytryptamine causes degeneration of the most distal serotoninergic axons.

Perinatal morphine exposure alters peptidergic development in the striatum.

It has been reported that perinatal exposure to opiates affects mRNA synthesis, body growth and brain development in mammals, including humans. We have observed that morphine administration in drinking water during the perinatal period alters peptide development in the striatum of the rat. There is a marked increase in substance P and met-enkephalin content, the latter is maintained even at 30 days postnatally.

Perinatal exposure to ethanol affects postnatal degeneration and regeneration of serotoninergic pathways in the spinal cord.

It has been reported that chronic ethanol exposure during intrauterine life may cause severe adverse effects in early infancy that have been termed fetal alcohol syndrome. These alterations may perturb the normal brain development as though alcohol exposure might have altered the basic cellular interrelationship underlying neuronal plasticity. The neonatal lesion of the serotoninergic pathways in the central nervous system with the selective neurotoxin 5,7-DHT supplies an ideal model for studying the effects of substances of abuse on degenerative and regenerative events.

Intraspinal degenerative atrophy caused by sciatic nerve lesions prevented by acetyl-L-carnitine.

Peripheral nerve lesions cause retrograde changes in the spinal cord, involving initially the descending serotoninergic pathways and later the substance P sensory input and methionine-enkephalin interneurons. Within 48 h after sciatic nerve resection there is a significant increase of 5-hydroxyindoleacetic acid in the lumbar spinal cord with no changes of serotonin metabolism in the cell body areas. The immunocytochemical analysis of the spinal cord shows that 20 days after nerve lesion there is a loss of substance P-positive boutons in the laminae I and II of the dorsal horn in the lumbar segment.

Peptide alterations in autonomic diabetic neuropathy prevented by acetyl-L-carnitine.

Autonomic neuropathy and gastrointestinal problems are among the most common complications of diabetes. In this report it is shown that a possible correlation between the two disorders might exist, since diabetes causes a profound alteration of the peptidergic innervation of the gut. It is reported that 14 weeks after diabetes induction with alloxan the levels of substance P and methionine-enkephalin are markedly reduced throughout the intestine, while vasoactive intestinal polypeptide content is dramatically increased.

Early neurochemical changes in the autonomic neuropathy of the gut in experimental diabetes.

Some neurochemical changes in the gut of rats after five weeks of alloxan-induced diabetes were investigated. It was found that at this stage of diabetes the changes were restricted mainly to the small intestine with a special selectivity for the duodenum. No changes were found in the most part of the large intestine and rectum.