Deep ocean minerals minimize eccentric exercise-induced inflammatory response of rat skeletal muscle.

Background: We have previously shown an accelerated recovery from muscle fatigue in men challenged by prolonged exercise after oral deep ocean minerals (DOM) supplementation. Here, we hypothesized a decrease in eccentric exercise-induced muscle inflammation in rats regularly consuming DOM-containing drinks (hardness 600 mg/L and fructose 11%). Methods: Forty-seven male Sprague Dawley rats were randomized into 4 groups: Control (C, N = 12), Fructose (F, N = 12), Fructose+Exercise (FE, N = 12), and Fructose+Exercise+DOM (FED, N = 11). Since fructose is a commonly used ingredient in beverages, 11% of fructose was added as a vehicle of the study. Soleus muscles of rats were analyzed 24 h after an acute bout of downhill running following 9 weeks of DOM supplementation. Results: Leukocyte infiltration and TNF-a mRNA of muscle in the FE group were 5 times and 4 times greater the F group, respectively, (P eight fold greater than the C group (P < 0.05). The reduced glutathione (GSH) of muscle in the F group was 34% lower than that in the C group (P < 0.05). However, GSH levels were similar for the C and FED groups. Conclusion: Prolonged fructose supplementation modulates inflammatory balance of rat skeletal muscle. The results of the study suggest that DOM can minimize eccentric exercise-induced inflammatory cytokine responses in rat skeletal muscle.This work was supported by grants from Taiwan Yes Corporation, Ministry of Science and Technology (Grant No. 102-2410-H-845-018-MY3), and University of Taipei. The funding sponsors had no role in the design of the study; in the collection, analyses, or interpretation of data; in the writing of the manuscript, and in the decision to publish the results

Population Receptive Field Dynamics in Human Visual Cortex

Seminal work in the early nineties revealed that the visual receptive field of neurons in cat primary visual cortex can change in location and size when artificial scotomas are applied. Recent work now suggests that these single neuron receptive field dynamics also pertain to the neuronal population receptive field (pRF) that can be measured in humans with functional magnetic resonance imaging (fMRI). To examine this further, we estimated the pRF in twelve healthy participants while masking the central portion of the visual field. We found that the pRF changes in location and size for two differently sized artificial scotomas, and that these pRF dynamics are most likely due to a combination of the neuronal receptive field position and size scatter as well as modulatory feedback signals from extrastriate visual areas

Visually Driven Activation in Macaque Areas V2 and V3 without Input from the Primary Visual Cortex

Creating focal lesions in primary visual cortex (V1) provides an opportunity to study the role of extra-geniculo-striate pathways for activating extrastriate visual cortex. Previous studies have shown that more than 95% of neurons in macaque area V2 and V3 stop firing after reversibly cooling V1 [1], [2], [3]. However, no studies on long term recovery in areas V2, V3 following permanent V1 lesions have been reported in the macaque. Here we use macaque fMRI to study area V2, V3 activity patterns from 1 to 22 months after lesioning area V1. We find that visually driven BOLD responses persist inside the V1-lesion projection zones (LPZ) of areas V2 and V3, but are reduced in strength by ∼70%, on average, compared to pre-lesion levels. Monitoring the LPZ activity over time starting one month following the V1 lesion did not reveal systematic changes in BOLD signal amplitude. Surprisingly, the retinotopic organization inside the LPZ of areas V2, V3 remained similar to that of the non-lesioned hemisphere, suggesting that LPZ activation in V2, V3 is not the result of input arising from nearby (non-lesioned) V1 cortex. Electrophysiology recordings of multi-unit activity corroborated the BOLD observations: visually driven multi-unit responses could be elicited inside the V2 LPZ, even when the visual stimulus was entirely contained within the scotoma induced by the V1 lesion. Restricting the stimulus to the intact visual hemi-field produced no significant BOLD modulation inside the V2, V3 LPZs. We conclude that the observed activity patterns are largely mediated by parallel, V1-bypassing, subcortical pathways that can activate areas V2 and V3 in the absence of V1 input. Such pathways may contribute to the behavioral phenomenon of blindsight

Surface-Based Analyses of Anatomical Properties of the Visual Cortex in Macular Degeneration

INTRODUCTION: Macular degeneration (MD) can cause a central visual field defect. In a previous study, we found volumetric reductions along the entire visual pathways of MD patients, possibly indicating degeneration of inactive neuronal tissue. This may have important implications. In particular, new therapeutic strategies to restore retinal function rely on intact visual pathways and cortex to reestablish visual function. Here we reanalyze the data of our previous study using surface-based morphometry (SBM) rather than voxel-based morphometry (VBM). This can help determine the robustness of the findings and will lead to a better understanding of the nature of neuroanatomical changes associated with MD. METHODS: The metrics of interest were acquired by performing SBM analysis on T1-weighted MRI data acquired from 113 subjects: patients with juvenile MD (JMD; n = 34), patients with age-related MD (AMD; n = 24) and healthy age-matched controls (HC; n = 55). RESULTS: Relative to age-matched controls, JMD patients showed a thinner cortex, a smaller cortical surface area and a lower grey matter volume in V1 and V2, while AMD patients showed thinning of the cortex in V2. Neither patient group showed a significant difference in mean curvature of the visual cortex. DISCUSSION: The thinner cortex, smaller surface area and lower grey matter volume in the visual cortex of JMD patients are consistent with our previous results showing a volumetric reduction in their visual cortex. Finding comparable results using two rather different analysis techniques suggests the presence of marked cortical degeneration in the JMD patients. In the AMD patients, we found a thinner cortex in V2 but not in V1. In contrast to our previous VBM analysis, SBM revealed no volumetric reductions of the visual cortex. This suggests that the cortical changes in AMD patients are relatively subtle, as they apparently can be missed by one of the methods

The N400 effect in children: relationships with comprehension, vocabulary and decoding.

Using event-related potentials (ERPs), we investigated the N400 (an ERP component that occurs in response to meaningful stimuli) in children aged 8-10 years old and examined relationships between the N400 and individual differences in listening comprehension, word recognition and non-word decoding. Moreover, we tested the claim that the N400 effect provides a valuable indicator of behavioural vocabulary knowledge. Eighteen children were presented with picture-word pairs that were either 'congruent' (the picture depicted the spoken word) or 'incongruent' (they were unrelated). Three peaks were observed in the ERP waveform triggered to the onset of the picture-word stimuli: an N100 in fronto-central channels, an N200 in central-parietal channels and an N400 in frontal, central and parietal channels. In contrast to the N100 peak, the N200 and N400 peaks were sensitive to semantic incongruency with greater peak amplitudes for incongruent than congruent conditions. The incongruency effects for each peak correlated positively with listening comprehension but when the peak amplitudes were averaged across congruent/incongruent conditions they correlated positively with non-word decoding. These findings provide neurophysiological support for the position that sensitivity to semantic context (reflected in the N400 effect) is crucial for comprehension whereas phonological decoding skill relates to more general processing differences reflected in the ERP waveform. There were no correlations between ERP and behavioural measures of expressive or receptive vocabulary knowledge for the same items, suggesting that the N400 effect may not be a reliable estimate of vocabulary knowledge in children aged 8-10 years

Treatment of age‐related macular degeneration with aflibercept using a treat, extend and fixed protocol; A 4‐year study of treatment outcomes, durability, safety and quality of life (An extension to the <scp>MATE</scp> randomised controlled trial)

AbstractPurposeData are limited pertaining to the long‐term benefits of aflibercept treatment for neovascular age‐related macular degeneration (nAMD). The aim of this study was to provide outcomes, safety, durability and quality‐of‐life data with aflibercept using a modified treat, extend and fixed regime over 4 years.MethodsProspective, multicentre, single cohort observational study of treatment‐naïve nAMD participants treated with aflibercept as 2‐year extension of the MATE‐trial that compared early and late Treat‐and‐Extend for 2 years. Refracted ETDRS best corrected visual acuity (BCVA), central retinal thickness (CRT), treatment interval and adverse events were assessed. Quality‐of‐life was measured using the Macular Disease Dependent Quality of Life (MacDQoL) and Macular Disease Treatment Satisfaction Questionnaires (MacTSQ).ResultsTwenty‐six of 40 participants completing the MATE‐trial were enrolled with 20 completing the total 4‐year study. Mean BCVA was 60.7 at Month 0 and 64.8 ETDRS letters at Month 48 while CRT decreased from 423.7 μm to 292.2 μm. Five participants discontinued treatment due to inactivity. The mean number of treatments and visits for the remaining participants was 27 and 30.0, respectively, with treatment intervals extended to 12 weeks in four participants at Month 48. Both AMD‐specific QoL and treatment satisfaction remained stable between Months 0 and 48 and mean BCVA significantly correlated with AMD‐specific QoL scores at Months 12, 24 and 48.ConclusionsResults suggest that BCVA can be maintained over 48 months when following a treat‐extend‐and‐fix regimen of aflibercept with intervals out to 12 weeks, while maintaining AMD‐specific QoL and treatment satisfaction.</jats:sec