305,359 research outputs found
Modulation of geraniol metabolism during alcohol fermentation
Geraniol is the main monoterpenol present in Gewurtztraminer white grapes and in some red aromatic grapes from northern Italy. During fermentation, the geraniol concentration showed a dramatic drop and a small amount was transformed into linalool and α-terpineol by an acid catalysed chemical reaction. Yeast are responsible for changing most of the geraniol to citronellol through enzymatic reactions. The final aroma of wine is due mainly to both the untransformed geraniol and the formed citronellol. In this study, competition between the geraniol-citronellol transformation and another metabolic process, in which according to our hypothesis sterol biosynthesis is involved, was investigated. Geraniol, in the active form of geranyl pyrophosphate, is one of intermediates in that metabolic pathway. The addition of ergosterol, one of final products of sterol biosynthesis, to the fermentation medium, appeared to reduce the amount of geraniol involved in this metabolic pathway; as a result geraniol-citronellol transformation was favoured. The result was a higher production of citronellol with the same geraniol consumption. The relationships between oxygen and regulation of the metabolic pathways involving geraniol were also studied. Results showed that aerobic conditions could improve citronellol production. Finally, it was observed that metabolism of geraniol also depended on the physiological state of the yeast during fermentation
Motor and Limbic System Contribution to Emotional Laughter across the Lifespan
Laughter is a universal human behavior generated by the cooperation of different systems toward the construction of an expressive vocal pattern. Given the sensitivity of neuroimaging techniques to movements, the neural mechanisms underlying laughter expression remain unclear. Herein, we characterized the neural correlates of emotional laughter using the onsets and the duration of laughter bursts to inform functional magnetic resonance imaging. Laughter-related blood oxygen level-dependent (BOLD) increases involved both the motor (motor cortex, supplementary motor area, frontal operculum) and the emotional/limbic (anterior cingulate cortex, amygdala, n. accumbens, hippocampus) systems, as well as modulatory circuitries encompassing the basal ganglia, thalamus, and cerebellum. BOLD changes related to the 2 s preceding the laughter outbreak were selectively observed at the temporo-occipital junction and the periaqueductal gray matter, supporting the role of the former in the detection of incongruity and the gating role of the latter in the initiation of spontaneous laughter. Moreover, developmental changes were identified in laughter processing, consisting in a greater engagement of the reward circuitry in younger subjects; conversely, the default mode network appears more activated in older participants. Our findings contribute valuable information about the processing of real-life humorous materials and suggest a close link between laughter-related motor, affective, and cognitive elements, confirming its complex and multi-faceted nature
Valproate Use Is Associated With Posterior Cortical Thinning and Ventricular Enlargement in Epilepsy Patients
Valproate is a drug widely used to treat epilepsy, bipolar disorder, and occasionally to prevent migraine headache. Despite its clinical efficacy, prenatal exposure to valproate is associated with neurodevelopmental impairments and its use in children and adults was associated with rare cases of reversible brain atrophy and ventricular enlargement. To determine whether valproate use is related with structural brain changes we examined through a cross-sectional study cortical and subcortical structures in a group of 152 people with epilepsy and a normal clinical brain MRI. Patients were grouped into those currently using valproate (n = 54), those taking drugs other than valproate (n = 47), and drug-naïve patients (n = 51) at the time of MRI, irrespectively of their epilepsy syndrome. Cortical thickness and subcortical volumes were analyzed using Freesurfer, version 5.0. Subjects exposed to valproate (either in mono- or polytherapy) showed reduced cortical thickness in the occipital lobe, more precisely in the cuneus bilaterally, in the left lingual gyrus, and in left and right pericalcarine gyri when compared to patients who used other antiepileptic drugs, to drug-naïve epilepsy patients, and to healthy controls. Considering the subgroup of patients using valproate monotherapy (n = 25), both comparisons with healthy controls and drug-naïve groups confirmed occipital lobe cortical thickness reduction. Moreover, patients using valproate showed increased left and right lateral ventricle volume compared to all other groups. Notably, subjects who were non-valproate users at the time of MRI, but who had valproate exposure in the past (n = 27) did not show these cortical or subcortical brain changes. Cortical changes in the posterior cortex, particularly in the visual cortex, and ventricular enlargement, are present in people with epilepsy using valproate, independently from clinical and demographical variables. These findings are relevant both for the efficacy and adverse events profile of valproate use in people with epilepsy
Regressive modifications of climbing fibres following Purkinje cell degeneration in the cerebellar cortex of the adult rat
The role of postsynaptic neurons in the maintenance of adult terminal axon arbours was investigated in the rat olivocerebellar system. The degeneration of Purkinje cells, the main target of olivary axons in the cerebellar cortex, was obtained by intraparenchymal application of kainate. The structural features of target-deprived climbing fibres, visualized by Phaseolus vulgaris leucoagglutinin tracing, were examined from two days to six months after the lesion. Following the degeneration of its Purkinje cell, the climbing fibre underwent remarkable regressive modifications involving the disappearance of most of the terminal arborization. Never the less, atrophic arbours still spanned through the molecular layer six months after the lesion. Morphometric evaluations showed that, one week after kainate application, total arbour length was already reduced to 52% of control, whereas the number of branches and of varicosities had both dropped around 40%. This retraction process progressed in the following stages to reach its maximum at about one month after the lesion, when total length was 30% of control and only 10% of branches and varicosities were still present. Only a slight tendency to a further decrease of the values could be detected at longer survival times. Branching pattern analysis revealed that such regressive phenomena mainly involved the distal compartment of the climbing fibres, the one made of fine varicose branchlets, while sparing the proximal thick branches. In addition, the whole process appeared to follow some rather strict guiding principles leading to an ordered branch retraction, from the periphery of the arbour inwards. Finally, in order to rule out the possibility that the observed changes could be due to a direct action of kainate on climbing fibres, we designed an alternative method of killing Purkinje cells by intraparenchymal injection of propidium iodide. The structural features of climbing fibres deprived of their target by such a procedure were very similar to those shown by arbours from time-matched kainate-lesioned animals at both qualitative and quantitative levels. Our results show that target deprivation induces remarkable structural modifications in the climbing fibre, leading to the retraction of most of the arbour. Never the less, the integrity of the Purkinje cell is not necessary for the maintenance of the whole arborization since its proximal compartment is maintained in the molecular layer for several months after target degeneration. It is proposed that the Purkinje cell, most likely by acting through a contact factor, directly controls the formation and the maintenance of the distal climbing fibre branches with their varicosities, which represent the presynaptic compartment of the axonal arbour
Going Beyond Counting First Authors in Author Co-citation Analysis
The present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation
counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings
are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that
only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into
account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed
Bayesian multi-modal model comparison: a case study on the generators of the spike and the wave in generalized spike–wave complexes
We present a novel approach to assess the networks involved in the generation of spontaneous pathological brain activity based on multi-modal imaging data. We propose to use probabilistic fMRI-constrained EEG source reconstruction as a complement to EEG-correlated fMRI analysis to disambiguate between networks that co-occur at the fMRI time resolution. The method is based on Bayesian model comparison, where the different models correspond to different combinations of fMRI-activated (or deactivated) cortical clusters. By computing the model evidence (or marginal likelihood) of each and every candidate source space partition, we can infer the most probable set of fMRI regions that has generated a given EEG scalp data window. We illustrate the method using EEG-correlated fMRI data acquired in a patient with ictal generalized spike–wave (GSW) discharges, to examine whether different networks are involved in the generation of the spike and the wave components, respectively. To this effect, we compared a family of 128 EEG source models, based on the combinations of seven regions haemodynamically involved (deactivated) during a prolonged ictal GSW discharge, namely: bilateral precuneus, bilateral medial frontal gyrus, bilateral middle temporal gyrus, and right cuneus. Bayesian model comparison has revealed the most likely model associated with the spike component to consist of a prefrontal region and bilateral temporal–parietal regions and the most likely model associated with the wave component to comprise the same temporal–parietal regions only. The result supports the hypothesis of different neurophysiological mechanisms underlying the generation of the spike versus wave components of GSW discharges
The resilient brain and the guardians of sleep: new perspectives on old assumptions
Resilience is the capacity of a system, enterprise or a person to maintain its core purpose and integrity in the face of dramatically changed circumstances. In human physiology, resilience is the capacity of adaptively overcoming stress and adversity while maintaing normal psychological and physical functioning. In this review, we investigate the resilient strategies of sleep. First, we discuss the concept of brain resilience, highlighting the modular structure of small-world networking, neuronal plasticity and critical brain behaviour. Second, we explore the contribution of sleep to brain resilience listing the putative factors that impair sleep quality and predict susceptibility to sleep disorders. The third part details the manifold mechanisms acting as guardians of sleep, i.e., homeostatic, circadian and ultradian processes, sleep microstructure (K-complexes, delta bursts, arousals, cyclic alternating pattern, spindles), gravity, muscle tone and dreams. Mapping and pooling together the guardians of sleep in a dynamic integrated framework might lead towards an objective measure of sleep resilience and identify effective personalized strategies (biological, pharmacological, behavioral) to restore or protect the core properties of healthy sleep
Generalized spike-and-wave discharges offset is related to precuneal-posterior cingulate activity.
Introduction: Recent EEG-fMRI studies revealed that a widespread neural network subserves the generation of ictal and interictal activity in patients with generalized epilepsy (1-4). Different studies investigated the hemodynamic changes related to the onset and duration of generalized spike-and-wave discharges (GSWD) in human epilepsy. Conversely, the BOLD signal changes related to GSWD termination has not been addressed to date. Few studies have focused the mechanisms that promote seizures stop at molecular and cellular level (6). In particular, a recent single neuron recording study in human focal epilepsy (7) revealed that neuronal firing patterns change homogeneously at seizure offset suggesting that seizure termination is marked by an abrupt homogeneous change in neuronal firing. These data support a mechanism that acts at the neural network level.
The present EEG-fMRI study aimed at evaluating the neural correlates of seizure termination studying the BOLD variations at GSWD offset in a large sample of patients with Idiopathic generalized epilepsy (IGE).
Materials and methods: eighteen patients (6 male; mean age 25 yrs.) with IGE were included. Scalp EEG was recorded by means of a 32 channels MRI-compatible EEG recording system. Functional data were acquired with a 3T Philips Intera System (TR=3000 ms) from 30 axial contiguous 4 mm slices (64 x 64 matrix) over two-three 10-min sessions per patient with continuous simultaneous video-EEG recording. Event-related analysis was performed with SPM8 software, using the following regressors: (1) GSWD onset and duration; (2) GSWD offset. Data were analyzed at a second level random effect analysis.
Results: a mean of 17 events for each patient was recorded (mean duration= 4 s). Second-level random effect analysis related to onset and GSWD length confirmed previous findings (5) revealing a thalamus activation and a parietal and precuneus-posterior cingulate deactivation. GSWD onset respect to the offset showed BOLD increases in the prefrontal regions (inferior and middle frontal gyrus) mostly on the left side and in the bilateral primary visual cortex. Conversely, GSWD offset respect to the onset revealed significant hemodynamic changes over the precuneus-posterior cingulate region (Fig. 1).
Conclusions: fMRI results showed that the neural network at GSWD termination involved precuneus-posterior cingulate region. These findings confirm an important role of this brain region in GSWD pathophysiology. Particularly, precuneal/posterior cingulate neuronal activity might participate actively to the GSWD termination or it might reflect the recovery of the awareness impaired during the pathological activity.
BIBLIOGRAFY
1) Gotman J, Grova C, Bagshaw A, Kobayashi E, Aghakhani Y, Dubeau F. (2005) Generalized epileptic discharges show thalamocortical activation and suspension of the default state of the brain. Proc Natl Acad Sci USA, vol. 102, pp. 15236–15240.
2) Moeller F, Siebner HR, Wolff S, Muhle H, Boor R, Granert O, Jansen O, Stephani U, Siniatchkin M. (2008) Changes in activity of striato-thalamo- cortical network precede generalized spike wave discharges. Neuroimage vol. 39, pp. 1839–1849.
3) Vaudano AE, Laufs H, Kiebel SJ, Carmichael DW, Hamandi K, Guye M, Thornton R, Rodionov R, Friston KJ, Duncan JS, Lemieux L. (2009) Causal hierarchy within the thalamo-cortical network in spike and wave discharges. PLoS ONE vol. 4:e6475.
4) Carney PW, Masterton RA, Harvey AS, Scheffer IE, Berkovic SF, Jackson GD. (2010) The core network in absence epilepsy. Differences in cortical and thalamic BOLD response. Neurology vol. 75, pp. 904–911.
5) Benuzzi F, Mirandola L, Pugnaghi M, Farinelli V, Tassinari CA, Capovilla G, Cantalupo G, Beccaria F, Nichelli P, Meletti S (2012). Increased cortical BOLD signal anticipates generalized spike and wave discharges in adolescents and adults with idiopathic generalized epilepsies. Epilepsia, vol. 53(4), pp. 622-30.
6) Fred A. Lado, Solomon L. Moshé (2008). How do seizures stop? Epilepsia, vol. 49 (10), pp. 1651–1664.
7) Wilson Truccolo,Jacob A Donoghue,Leigh R Hochberg, Emad N Eskandar, Joseph R Madsen, William S Anderson, Emery N Brown, Eric Halgren, Sydney S Cash (2011). Single-neuron dynamics in human focal epilepsy, Nature Neuroscience,vol. 14 (5), pp. 635-641
Intracranial time–frequency correlates of seizure-related negative BOLD response in the sensory-motor network
The study evaluates the BOLD signal related to high and low frequency EEG changes related to focal seizures in the motor syste
Cortical and subcortical brain alterations in Juvenile Absence Epilepsy
Despite the common assumption that genetic generalized epilepsies are characterized by a macroscopically normal brain on magnetic resonance imaging, subtle structural brain alterations have been detected by advanced neuroimaging techniques in Childhood Absence Epilepsy syndrome. We applied quantitative structural MRI analysis to a group of adolescents and adults with Juvenile Absence Epilepsy (JAE) in order to investigate micro-structural brain changes using different brain measures. We examined grey matter volumes, cortical thickness, surface areas, and subcortical volumes in 24 patients with JAE compared to 24 healthy controls; whole-brain voxel-based morphometry (VBM) and Freesurfer analyses were used. When compared to healthy controls, patients revealed both grey matter volume and surface area reduction in bilateral frontal regions, anterior cingulate, and right mesial-temporal lobe. Correlation analysis with disease duration showed that longer disease was correlated with reduced surface area in right pre- and post-central gyrus. A possible effect of valproate treatment on brain structures was excluded. Our results indicate that subtle structural brain changes are detectable in JAE and are mainly located in anterior nodes of regions known to be crucial for awareness, attention and memory
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