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A pair of reference-quality seashore snake genomes expose their divergent evolution involving versatile features along with venom programs.
agement might be an important mechanism leading to overlapping fixations. Our new analysis of the visual exploration area, based on foveal vision, may be a promising additional approach in visual attention research. It allows to accurately measure the portion of the picture that was effectively explored, disentangle single from overlapping fixations, and distinguish between capture and re-capture fixations. Copyright © 2020 Kaufmann, Knobel, Nef, Müri, Cazzoli and Nyffeler.Behavioral disorders affect most diabetic patients and Zinc (Zn) has been used among adjuvant therapies for involvement in the etiology of depression and anxiety, however, the results are still controversial. The objective of this study was to compare the antidepressant, anxiolytic and neuroprotective activity of the supplementation of two Zn compounds in an animal model of Diabetes Mellitus type 1 (DM1). Thirty-eight (38) adult rats were randomized into four groups Control (C; n = 8); Diabetic (D; n = 10); Diabetic Zn Sulfate Supplement (DSZ; n = 10) and Diabetic Zn Gluconate Supplement (DGZ; n = 10). The DSZ group received Zn sulfate supplementation and the DGZ group received Zn gluconate supplementation at a dose of 15 mg/kg for 4 weeks. Data (mean ±SEM) were analyzed by the Mann-Whitney test with a significance level of p less then 0.05. The results indicate that Zn gluconate supplementation in diabetic animals presented an antidepressant effect demonstrated through the results obtained in the Forced Swim Test, and neuroprotective effect by attenuating alterations in the cerebral cortex; while Zn sulfate supplementation in diabetic animals showed an anxiolytic effect demonstrated by the results obtained in the open field test and the elevated plus maze test. Considering the set of results, supplementation with both zinc compounds showed neurobehavioral benefits in diabetic animals with different effects depending on the type of anion associated with Zn. Copyright © 2020 Cavalcanti, Gonçalves, Alves, Araújo, Carvalho, Lins, Alves, Soares, Pordeus and Aquino.Background Alzheimer's disease (AD) and diabetes mellitus (DM) often coexist in patients because having one of these conditions increases risk for the other. These two diseases share several pathophysiological mechanisms, such as specific inflammatory signaling pathways, oxidative stress, and cell apoptosis. It is still unclear exactly which mechanisms associated with DM are responsible for increased AD risk. Studies have found that even transient elevation of brain Aβ levels can allow T2DM to slightly disrupt the neural milieu in a way that encourages pathologies associated with the onset of memory deficits and AD. A recent study argues that a potential common pathogenetic mechanism underlying both DM and AD is evidenced by the cooccurrence of amyloid brain legions and deposits containing both tau and Aβ in pancreatic β cells. Given these links, an investigation detailing disease mechanisms as well as treatment options for patients with cooccurring DM and AD is urgently needed. The biological effects of resveratrol relevant to DM and AD treatment include its abilities to modulate oxidative stress and reduce inflammation. A rat model of DM and concomitant AD was created for this study using intraperitoneal injection of streptozotocin and hippocampal injection of Aβ1-40 to characterize resveratrol's potential protective action. Results Resveratrol significantly increased the Sirt1 expression, inhibited the memory impairment, the increased acetylcholinesterase, malondialdehyde, interleukin-1β and interleukin 6 levels, and the decreased levels of choline acetyltransferase (ChAT), superoxide dismutase (SOD), and glutathione in this rat model of diabetes and concomitant AD. The Sirt 1 inhibitor EX527 partially reversed the effects of resveratrol. Conclusion This study suggests that resveratrol may have a neuroprotective action through activation of Sirt1 signaling in diabetes and AD with concurrent onset. Copyright © 2020 Ma, Sun, Han, Li, Jiang, Chen, Zhang and Lu.Alpha-synuclein (α-syn) is localized in cellular organelles of most neurons, but many of its physiological functions are only partially understood. α-syn accumulation is associated with Parkinson's disease, dementia with Lewy bodies, and multiple system atrophy as well as other synucleinopathies; however, the exact pathomechanisms that underlie these neurodegenerative diseases remain elusive. In this review, we describe what is known about α-syn function and pathophysiological changes in different cellular structures and organelles, including what is known about its behavior as a prion-like protein. We summarize current knowledge of α-syn and its pathological forms, covering its effect on each organelle, including aggregation and toxicity in different model systems, with special interest on the mitochondria due to its relevance during the apoptotic process of dopaminergic neurons. Moreover, we explore the effect that α-syn exerts by interacting with chromatin remodeling proteins that add or remove histone marks, up-regulate its own expression, and resume the impairment that α-syn induces in vesicular traffic by interacting with the endoplasmic reticulum. We then recapitulate the events that lead to Golgi apparatus fragmentation, caused by the presence of α-syn. Finally, we report the recent findings about the accumulation of α-syn, indirectly produced by the endolysosomal system. In conclusion, many important steps into the understanding of α-syn have been made using in vivo and in vitro models; however, the time is right to start integrating observational studies with mechanistic models of α-syn interactions, in order to look at a more complete picture of the pathophysiological processes underlying α-synucleinopathies. Copyright © 2020 Bernal-Conde, Ramos-Acevedo, Reyes-Hernández, Balbuena-Olvera, Morales-Moreno, Argüero-Sánchez, Schüle and Guerra-Crespo.We hypothesized that a single-leg version of the Hybrid Assistive Limb (HAL) system could improve the gait and physical function of patients with hemiparesis following a stroke. SZL P1-41 In this pilot study, we therefore compared the efficacy of HAL-based gait training with that of conventional gait training (CGT) in patients with acute stroke. Patients admitted to the participating university hospital were assigned to the HAL group, whereas those admitted to outside teaching hospitals under the same rehabilitation program who did not use the HAL were assigned to the control group. Over 3 weeks, all participants completed nine 20 min sessions of gait training, using either HAL (i.e., the single-leg version of HAL on the paretic side) or conventional methods (i.e., walking aids and gait orthoses). Outcome measures were evaluated before and after the nine training sessions. The Functional Ambulation Category (FAC) was the primary outcome measure, but the following secondary outcome measures were also assessed National Ia, Takada, Tsukada, Fujimori, Sato, Maruo, Kawamoto, Hada, Yamazaki, Sankai, Ishikawa, Matsumaru and Matsumura.Aim We initially developed concurrent recording of muscle sympathetic nerve activity (MSNA) and functional magnetic resonance imaging (fMRI) of the brain to functionally identify the human homolog of the rostral ventrolateral medulla (RVLM). Here we summarize the cortical and subcortical connections to the RVLM, as identified using MSNA-coupled fMRI. Methods MSNA was recorded via tungsten microelectrodes inserted into the peroneal nerve. Gradient echo, echo-planar fMRI was performed at 3T (Philips Achieva). 200 volumes (46 axial slices (TR = 8 s, TE = 4 s, flip angle = 90°, raw voxel size = 1.5 × 1.5 × 2.75 mm) were collected in a 4 s-ON, 4 s-OFF sparse sampling protocol and MSNA measured in each 1 s epoch in the 4-s period between scans. Blood oxygen level dependent (BOLD) signal intensity was measured in the corresponding 1 s epoch 4 s later to account for peripheral neural conduction and central neurovascular coupling delays. Results BOLD signal intensity was positively related to bursts of MSNA in the RVLtion of spontaneous bursts of MSNA and their augmentation during physiological and pathophysiological increase in vasoconstrictor drive. Copyright © 2020 Macefield and Henderson.Using advanced virtual reality technology, we demonstrate that exposure to virtual inclinations visually simulating inclined walking induces gait modulations in a manner consistent with expected gravitational forces (i.e., acting upon a free body), suggesting vision-based perception of gravity. The force of gravity critically impacts the regulation of our movements. However, how humans perceive and incorporate gravity into locomotion is not well understood. In this study, we introduce a novel paradigm for exposing humans to incongruent sensory information under conditions constrained by distinct gravitational effects, facilitating analysis of the consistency of human locomotion with expected gravitational forces. Young healthy adults walked under conditions of actual physical inclinations as well as virtual inclinations. We identify and describe 'braking' and 'exertion' effects - locomotor adaptations accommodating gravito-inertial forces associated with physical inclines. We show that purely visual cues (from virtual inclinations) induce consistent locomotor adaptations to counter expected gravity-based changes, consistent with indirect prediction mechanisms. Specifically, downhill visual cues activate the braking effect in anticipation of a gravitational boost, whereas uphill visual cues promote an exertion effect in anticipation of gravitational deceleration. Although participants initially rely upon vision to accommodate environmental changes, a sensory reweighting mechanism gradually reprioritizes body-based cues over visual ones. A high-level neural model outlines a putative pathway subserving the observed effects. Our findings may be pivotal in designing virtual reality-based paradigms for understanding perception and action in complex environments with potential translational benefits. Copyright © 2020 Cano Porras, Zeilig, Doniger, Bahat, Inzelberg and Plotnik.Deep brain stimulation (DBS) is a well-established technique for the treatment of movement and psychiatric disorders through the modulation of neural oscillatory activity and synaptic plasticity. The central thalamus (CT) has been indicated as a potential target for stimulation to enhance memory. However, the mechanisms underlying local field potential (LFP) oscillations and memory enhancement by CT-DBS remain unknown. In this study, we used CT-DBS to investigate the mechanisms underlying the changes in oscillatory communication between the CT and hippocampus, both of which are involved in spatial working memory. Local field potentials (LFPs) were recorded from microelectrode array implanted in the CT, dentate gyrus, cornu ammonis (CA) region 1, and CA region 3. Functional connectivity (FC) strength was assessed by LFP-LFP coherence calculations for these brain regions. In addition, a T-maze behavioral task using a rat model was performed to assess the performance of spatial working memory. In DBS group, our results revealed that theta oscillations significantly increased in the CT and hippocampus compared with that in sham controls. As indicated by coherence, the FC between the CT and hippocampus significantly increased in the theta band after CT-DBS. Moreover, Western blotting showed that the protein expressions of the dopamine D1 and α4-nicotinic acetylcholine receptors were enhanced, whereas that of the dopamine D2 receptor decreased in the DBS group. In conclusion, the use of CT-DBS resulted in elevated theta oscillations, increased FC between the CT and hippocampus, and altered synaptic plasticity in the hippocampus, suggesting that CT-DBS is an effective approach for improving spatial working memory. Copyright © 2019 Chang, Lo, Lin, Yang, Lin, Lin, Li, Hsieh, Ro, Chung, Chang, Lee, Kuo, Chen and Chen.
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