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Cervical discogenic pain (CDP) is mainly induced by cervical disc degeneration. However, how CDP modulates the functional interactions within the pain network remains unclear. In the current study, we studied the changed resting-state functional connectivities of pain network with 40 CDP patients and 40 age-, gender-matched healthy controls. We first defined the pain network with the seeds of the posterior insula (PI). Then, whole brain and seed-to-target functional connectivity analyses were performed to identify the differences in functional connectivity between CDP and healthy controls. Finally, correlation analyses were applied to reveal the associations between functional connectivities and clinical measures. Whole-brain functional connectivity analyses of PI identified increased functional connectivity between PI and thalamus (THA) and decreased functional connectivity between PI and middle cingulate cortex (MCC) in CDP patients. this website Functional connectivity analyses within the pain network further revealed increased functional connectivities between bilateral PI and bilateral THA, and decreased functional connectivities between left PI and MCC, between left postcentral gyrus (PoCG) and MCC in CDP patients. Moreover, we found that the functional connectivities between right PI and left THA, between left PoCG and MCC were negatively and positively correlated with the visual analog scale, respectively. Our findings provide direct evidence of how CDP modulates the pain network, which may facilitate understanding of the neural basis of CDP.The stress response is an important tool in an organism's ability to properly respond to adverse environmental conditions in order to survive. Intense acute or chronic elevation of glucocorticoids, a class of stress hormone, can have deleterious neurological effects, however, including memory impairments and emotional disturbances. In recent years, the protective role of the antioxidant micronutrient selenium against the negative impact of externally applied stress has begun to come to light. In this review, we will discuss the effects of stress on the brain, with a focus on glucocorticoid action in the hippocampus and cerebral cortex, and emerging evidence of an ability of selenium to normalize neurological function in the context of various stress and glucocorticoid exposure paradigms in rodent models.
Fetal growth restriction (FGR) has been associated with a higher risk of developing adverse perinatal outcomes and distinct neurodevelopmental and neurobehavioral disorders. The aim of the present study was to investigate the impact of prenatal food restriction on the brain proteome in both FGR and appropriately grown rats and to identify potential pathways connecting maternal malnutrition with altered brain development.
Ten time-dated pregnant Wistar rats were housed individually at their 12th day of gestation. On the 15th day of gestation, the rats were randomly divided into two groups, namely the food restricted one (
= 6) and the control group (
= 4). From days 15 to 21 the control group had unlimited access to food and the food restricted group was given half the amount of food that was on average consumed by the control group, based on measurements taken place the day before. On the 21st day of gestation, all rats delivered spontaneously and after birth all newborn pups of the food restricted gr chronic stress, poor memory and learning outcomes. Furthermore, this study highlighted that not only FGR, but also appropriately grown pups, which have been exposed to prenatal food deprivation may be at increased risk for impaired cognitive and developmental outcomes.
This study demonstrated that in both FGR and non-FGR neonates, a range of adaptive neurodevelopmental processes takes place, which may result in altered cellular morphology, chronic stress, poor memory and learning outcomes. Furthermore, this study highlighted that not only FGR, but also appropriately grown pups, which have been exposed to prenatal food deprivation may be at increased risk for impaired cognitive and developmental outcomes.Alzheimer's disease (AD) is the most common type of neurodegenerative disease leading to dementia in the elderly. Increasing evidence indicates that folate plays an important role in the pathogenesis of AD. To investigate the role of folate deficiency/possible deficiency in the risk of AD and the benefical effect of sufficient folate intake on the prevention of AD, a systematic review and meta-analysis were performed. The Web of Science, PubMed, CENTRAL, EBSCO, CNKI, CQVIP, and Wanfang databases were searched. The analysis of cross-sectional studies showed that the standardized mean difference (SMD) was -0.60 (95% confidence interval (CI) -0.65, -0.55), indicating that plasma/serum folate level is lower in AD patients than that in controls. Moreover, the combined odds ratio (OR) of case-control studies was 0.96 (95% CI 0.93, 0.99), while the combined ORs were 0.86 (95% CI 0.46, 1.26) and 1.94 (95% CI 1.02, 2.86) in populations with normal levels of folate (≥13.5 nmol/L) and folate deficiency/possible deficiency ( less then 13.5 nmol/L), respectively. In addition, the risk ratio (RR) of the cohort studies was 1.88 (95% CI 1.20, 2.57) in populations with folate deficiency/possible deficiency. Furthermore, when the intake of folate was equal to or higher than the recommended daily allowance, the combined RR and hazard ratio (HR) were 0.44 (95% CI 0.18, 0.71) and 0.76 (95% CI 0.52, 0.99), respectively. These results indicate that folate deficiency/possible deficiency increases the risk for AD, while sufficient intake of folate is a protective factor against AD.The mammalian circadian clock systems regulate the day-night variation of several physiological functions such as the sleep/wake cycle and core body temperature. Disturbance in the circadian clock due to shiftwork and chronic jetlag is related to the risk of several disorders such as metabolic syndrome and cancer. Recently, it has been thought that shiftwork increases the risk of sarcopenia which is characterized by age-related decline of muscle mass and its dysfunctions including muscle strength and/or physical performance. First, we summarize the association between circadian rhythm and the occurrence of sarcopenia and discuss its mechanistic insight by focusing on the muscle function and molecular clock gene in knockout or mutant mice. The clock gene knockout or mutant mice showed early aging phenotypes, including low survival rate and muscle loss. It suggests that improvement in the disturbance of the circadian clock plays an important role in the aging process of healthy muscles. Nutritional intake has the potential to augment muscle growth and entrain the peripheral clock. Second, we discuss the potential of chrono-nutrition in preventing aging-related muscle loss and dysfunction. We also focus on the effects of time-restricted feeding (TRF) and the distribution of protein intake across three meals.
Numerous task-based functional magnetic resonance imaging studies indicate the presence of compensatory functional improvement in patients with congenital cataracts. However, there is neuroimaging evidence that shows decreased sensory perception or cognition information processing related to visual dysfunction, which favors a general loss hypothesis. This study explored the functional connectivity between visual and other networks in children with congenital cataracts using resting state electroencephalography.
Twenty-one children with congenital cataracts (age 8.02 ± 2.03 years) and thirty-five sex- and age-matched normal sighted controls were enrolled to investigate functional connectivity between the visual cortex and the default mode network, the salience network, and the cerebellum network during resting state electroencephalography (eyes closed) recordings.
The congenital cataract group was less active, than the control group, in the occipital, temporal, frontal and limbic lobes in the theta, alphrtex and salience network might reflect attenuated inhibitory information flow, leading to higher attentional states, which could contribute to adaptation of environmental change in this group of patients.Nano-oscillators based on phase-transition materials are being explored for the implementation of different non-conventional computing paradigms. In particular, vanadium dioxide (VO2) devices are used to design autonomous non-linear oscillators from which oscillatory neural networks (ONNs) can be developed. In this work, we propose a new architecture for ONNs in which sub-harmonic injection locking (SHIL) is exploited to ensure that the phase information encoded in each neuron can only take two values. In this sense, the implementation of ONNs from neurons that inherently encode information with two-phase values has advantages in terms of robustness and tolerance to variability present in VO2 devices. Unlike conventional interconnection schemes, in which the sign of the weights is coded in the value of the resistances, in our proposal the negative (positive) weights are coded using static inverting (non-inverting) logic at the output of the oscillator. The operation of the proposed architecture is shown for pattern recognition applications.In this work the impact of two widely used anesthetics on the electrical activity of auditory brainstem neurons was studied during postnatal development. Spontaneous electrical activity in neonate rats of either sex was analyzed through a ventral craniotomy in mechanically ventilated pups to carry out patch clamp and multi-electrode electrophysiology recordings in the medial region of the superior olivary complex (SOC) between birth (postnatal day 0, P0) and P12. Recordings were obtained in pups anesthetized with the injectable mix of ketamine/xylazine (K/X mix), with the volatile anesthetic isoflurane (ISO), or in pups anesthetized with K/X mix that were also exposed to ISO. The results of patch clamp recordings demonstrate for the first time that olivary and periolivary neurons in the medial region of the SOC fire bursts of action potentials. The results of multielectrode recordings suggest that the firing pattern of single units recorded in K/X mix is similar to that recorded in ISO anesthetized rat pups. Taken together, the results of this study provide a framework to use injectable and volatile anesthetics for future studies to obtain functional information on the activity of medial superior olivary neurons in vivo.Recent studies examining the neurobiology of substance abuse have revealed a significant role of neuroimmune signaling as a mechanism through which drugs of abuse induce aberrant changes in synaptic plasticity and contribute to substance abuse-related behaviors. Immune signaling within the brain and the periphery critically regulates homeostasis of the nervous system. Perturbations in immune signaling can induce neuroinflammation or immunosuppression, which dysregulate nervous system function including neural processes associated with substance use disorders (SUDs). In this review, we discuss the literature that demonstrates a role of neuroimmune signaling in regulating learning, memory, and synaptic plasticity, emphasizing specific cytokine signaling within the central nervous system. We then highlight recent preclinical studies, within the last 5 years when possible, that have identified immune mechanisms within the brain and the periphery associated with addiction-related behaviors. Findings thus far underscore the need for future investigations into the clinical potential of immunopharmacology as a novel approach toward treating SUDs.
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