Falkenbergsanders0016

Expectations about forthcoming visual motion shaped by observers' experiences are known to induce anticipatory smooth eye movements (ASEMs) and changes in visual perception. Previous studies have demonstrated discrete effects of expectations on the control of ASEM and perception. However, the tasks designed in those studies were not able to segregate the effects of expectations and execution of ASEM itself on perception. In the present study, we attempted to directly examine the effect of ASEM itself on visual speed perception with a two-alternative forced-choice (2AFC) task, in which observers were asked to track a pair of sequentially presented visual motion stimuli with their eyes and to judge whether the second stimulus (test stimulus) was faster or slower than the first (reference stimulus). Our results showed that observers' visual speed perception, quantified by a psychometric function, shifted according to ASEM velocity. This was the case even though there was no difference in the steady-state eye velocity. Further analyses revealed that the observers' perceptual decisions could be explained by a difference in the magnitude of retinal slip velocity in the initial phase of ocular tracking when the reference and test stimuli were presented, rather than in the steady-state phase. Our results provide psychophysical evidence of the importance of initial ocular tracking in visual speed perception and the strong impact of ASEM.NEW & NOTEWORTHY We provide psychophysical evidence that the execution of anticipatory smooth eye movement (ASEM) leads to underestimation of visual speed perception, that is, observers perceive the object motion velocity as slower than when ASEM is not induced, even though the performance of subsequent ocular tracking is comparable. Moreover, our results showed that such perceptual decisions regarding object motion velocity were derived from the ASEM-induced decrease in retinal slip velocity during the initial phase of ocular tracking.The regulation of sleep/wake behavior and energy homeostasis is maintained in part by the hypothalamic neuropeptide orexin A (OXA, hypocretin). Reduction in orexin signaling is associated with sleep disorders and obesity, whereas higher lateral hypothalamic (LH) orexin signaling and sensitivity promotes obesity resistance. Similarly, dysregulation of hypothalamic neural networks is associated with onset of age-related diseases, including obesity and several neurological diseases. Despite the association of obesity and aging, and that adult populations are the target for the majority of pharmaceutical and obesity studies, conventional models for neuronal networks utilize embryonic neural cultures rather than adult neurons. Synchronous activity describes correlated changes in neuronal activity between neurons and is a feature of normal brain function, and is a measure of functional connectivity and final output from a given neural structure. Earlier studies show alterations in hypothalamic synchronicity followiation of OXA enhanced wakefulness in rats, indicating that OXA enhances wakefulness partly by promoting neural synchrony in the hypothalamus.NEW & NOTEWORTHY This study, for the first time, demonstrates that adult hypothalamic cultures are viable in vitro for a prolonged duration and are electrophysiologically active. In addition, the study shows that orexin enhances neural synchronization in adult hypothalamic cultures.Introduction Aberrant left hepatic artery (ALHA) can exist in up to 25% of the population. The presence of ALHA during lymph node (LN) dissection in gastric cancer may complicate the process. In this study, we aimed to evaluate the existence rate, management, and consequences of ALHA in our laparoscopic gastrectomy series. Patients and Methods Demographical and clinical data of laparoscopically operated 158 consecutive gastric cancer patients were collected retrospectively. Study patients were divided into three groups according to absence, existence and preservation, and existence and sacrification of ALHA. Harvested LN numbers, operation time, and postoperative alanine aminotransferase (ALT), aspartate aminotransferase (AST), and lactate dehydrogenase values on consecutive days were analyzed using Kruskal-Wallis and Mann-Whitney U tests. P  less then  .05 is accepted as significant. find more Results The median AST and ALT values of the ALHA-sacrificed group were higher than those of the group without ALHA and the ALHA-preserved group on the 1st, 3rd, and 5th postoperative days (P  less then  .05). On the 10th day, liver enzymes returned to normal values. Conclusion Adequate and appropriate dissection of LNs while preserving ALHA can be performed without prolonging the operation time. Sacrification of ALHA causes an increase in liver enzymes, with spontaneous recovery in most cases.Human upright balance is maintained through feedback mechanisms that use a variety of sensory modalities. Vision senses information about the position and velocity of the visual surround motion to improve balance by reducing the sway evoked by external disturbances. This study characterized the effects of visual information on human anterior-posterior body sway in upright stance by presenting perturbations through a virtual reality system. This made it possible to use a new visual perturbation signal, based on trapezoidal velocity pulses, whose amplitude and velocity could be controlled separately. To date, the influences of visual field position and velocity have only been studied independently due to the experimental limitations. The hip displacement, ankle torques, shank angles, and surface EMGs of four major ankle muscles were measured bilaterally as outputs. We found that the root mean square (RMS) hip displacement (body angle) increased systematically with visual input amplitude. However, for each ampliidal velocity pulses whose peak-to-peak amplitude and velocity could be modulated independently. Subsequently, we investigated how the amplitude and velocity of visual field motion influence the postural responses evoked in healthy adults.The cercal sensory system of cricket mediates the detection, localization, and identification of air current signals generated by predators, mates, and competitors. This mechanosensory system has been used extensively for experimental and theoretical studies of sensory coding at the cellular and system levels. It is currently thought that sensory interneurons (INs) in the terminal abdominal ganglion extract information about the direction, velocity, and acceleration of the air currents in the animal's immediate environment and project a coarse-coded representation of those parameters to higher centers. All feature detection is thought to be carried out in higher ganglia by more complex, specialized circuits. We present results that force a substantial revision of current hypotheses. Using multiple extracellular recordings and a special sensory stimulation device, we demonstrate that four well-studied interneurons in this system respond with high sensitivity and selectivity to complex dynamic multidirectional as shown in previous studies, these interneurons are also responsive to very small-scale, directionally complex air current waveforms. This feature sensitivity can be understood in terms of the cells' complex dendritic branching patterns.Methane has been proposed as an exoplanet biosignature. Imminent observations with the James Webb Space Telescope may enable methane detections on potentially habitable exoplanets, so it is essential to assess in what planetary contexts methane is a compelling biosignature. Methane’s short photochemical lifetime in terrestrial planet atmospheres implies that abundant methane requires large replenishment fluxes. While methane can be produced by a variety of abiotic mechanisms such as outgassing, serpentinizing reactions, and impacts, we argue that—in contrast to an Earth-like biosphere—known abiotic processes cannot easily generate atmospheres rich in CH4 and CO2 with limited CO due to the strong redox disequilibrium between CH4 and CO2. Methane is thus more likely to be biogenic for planets with 1) a terrestrial bulk density, high mean-molecular-weight and anoxic atmosphere, and an old host star; 2) an abundance of CH4 that implies surface fluxes exceeding what could be supplied by abiotic processes; and 3) atmospheric CO2 with comparatively little CO.Inositol pyrophosphates, such as 5-diphosphoinositol pentakisphosphate (IP7), are generated by a family of inositol hexakisphosphate kinases (IP6Ks), of which IP6K2 has been implicated in various cellular functions including neuroprotection. Absence of IP6K2 causes impairment of oxidative phosphorylation regulated by creatine kinase-B. In the present study, we show that IP6K2 is involved in attenuation of PINK1-mediated mitochondrial autophagy (mitophagy) in the brain. Up-regulation of dynamin-related protein (Drp-1), as well as increased expression of mitochondrial biogenesis markers (PGC1-α and NRF-1) in the cerebella of IP6K2-deleted mice (IP6K2-knockout), point to the involvement of IP6K2 in the regulation of mitochondrial fission. Knockdown of IP6K2 also leads to augmented glycolysis, potentially as a compensatory mechanism for decreased mitochondrial respiration. Overexpressing IP6K2 as well as IP6K2-kinase dead mutant in IP6K2-knockdown N2A cells reverses the expression of mitophagy markers, demonstrating that IP6K2-induced mitoprotection is catalytically/kinase independent. IP6K2 supplementation in K2-PINK1 double-knockdown N2A cells fails to reverse the expression of the mitophagic marker, LC3-II, indicating that the mitoprotective effect of IP6K2 is dependent on PINK1. Overall, our study reveals a key neuroprotective role of IP6K2 in the prevention of PINK1-mediated mitophagy in the brain.The receptor for colony stimulating factor 1 (CSF-1R) is important for the survival and function of myeloid cells that mediate pathology during experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis (MS). CSF-1 and IL-34, the ligands of CSF-1R, have similar bioactivities but distinct tissue and context-dependent expression patterns, suggesting that they have different roles. This could be the case in EAE, given that CSF-1 expression is up-regulated in the CNS, while IL-34 remains constitutively expressed. We found that targeting CSF-1 with neutralizing antibody halted ongoing EAE, with efficacy superior to CSF-1R inhibitor BLZ945, whereas IL-34 neutralization had no effect, suggesting that pathogenic myeloid cells were maintained by CSF-1. Both anti–CSF-1 and BLZ945 treatment greatly reduced the number of monocyte-derived cells and microglia in the CNS. However, anti–CSF-1 selectively depleted inflammatory microglia and monocytes in inflamed CNS areas, whereas BLZ945 depleted virtually all myeloid cells, including quiescent microglia, throughout the CNS. Anti–CSF-1 treatment reduced the size of demyelinated lesions and microglial activation in the gray matter. Lastly, we found that bone marrow–derived immune cells were the major mediators of CSF-1R–dependent pathology, while microglia played a lesser role. Our findings suggest that targeting CSF-1 could be effective in ameliorating MS pathology, while preserving the homeostatic functions of myeloid cells, thereby minimizing risks associated with ablation of CSF-1R–dependent cells.