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Baby Cerebral Sinovenous Thrombosis and Dural Sinus Malformation.
In addition, a significant decrease in the number of survived neurons was observed in both Ovx and Dia groups, while AChE activity was lower only in the Dia group. The Ovx + Dia group showed stronger apoptosis-induced neuropathology and inhibition of AChE activity. Treadmill exercise attenuated apoptosis-induced neuropathology in the Ovx and Dia groups and recovered AChE activity in the Dia group. Neuroprotective effects of treadmill exercise were mediated by inhibition of apoptosis. Moderate exercise protocol had no beneficial anti-apoptotic and neuroprotective effects in ovariectomized-diabetic rats.Ubiquitin-specific protease 22 (USP22), a potential marker of cancer stem cells, significantly influences stem cell fate choices. However, its functions in neural stem cells (NSCs) and adult neurogenesis, especially following traumatic brain injury (TBI), remain only partially understood. Here, we found that aberrant USP22 expression could affect NSC proliferation and stemness maintenance, as assessed by the generation of neurospheres, cell counting kit-8 (CCK-8) and immunofluorescence staining in vitro. Moreover, USP22 depletion promotes the differentiation of NSCs, both in vitro and in vivo. In contrast, USP22 overexpression inhibits NSC differentiation into neurons. Interestingly, our data showed that USP22 promotes the proliferation but inhibits the differentiation of NSCs in the dentate gyrus (DG) of the hippocampus soon after TBI. The Morris water maze (MWM) test was adopted to evaluate neurological function, which confirmed that USP22 could improve the learning and memory capacity that was already compromised following TBI. Overall, this study uncovers a potentially novel regulatory role of USP22 in the proliferation and differentiation ability of NSCs, contributing to the hippocampus-dependent cognitive function of TBI mice and may be a novel target for future therapeutic approaches.Microglia, the dynamic innate immune cells of the central nervous system, become activated in epilepsy. The process of microglial activation in epilepsy results in the creation of an inflammatory environment around the site of seizure onset, which contributes to the epileptogenic process and epilepsy progression. Cannabidiol (CBD) has been effective for use as an adjunctive treatment for two severe pediatric seizure disorders. Newly recognized as an Food and Drug Administration (FDA)-approved drug treatment in epilepsy, it has gained in popularity primarily for pain management. Although CBD is readily available in stores and online retailers, its mechanism of action and specifically its effects on microglia and their functions are yet fully understood. In this study, we examine the effects of commercially available CBD on microglia inflammatory activation and neurogenic response, in the presence and absence of seizures. We use systemic administration of kainate to elicit seizures in mice, which are assessed behaviorally. Artisanal CBD is given in different modes of administration and timing to dissect its effect on seizure intensity, microglial activation and aberrant seizure-related neurogenesis. CBD significantly dampens microglial migration and accumulation to the hippocampus. While long term artisanal CBD use does not prevent or lessen seizure severity, CBD is a promising adjunctive partner for its ability to depress epileptogenic processes. These studies indicate that artisanal CBD is beneficial as it both decreases inflammation in the CNS and reduces the number of ectopic neurons deposited in the hippocampal area post seizure.Several factors, including environmental modifications, stimulate neuroplasticity. One type of neuroplasticity consists in the generation of new neurons in the dentate gyrus of the hippocampus. Neurogenesis is modulated by environmental enrichment (ENR, tunnels plus running wheel) and affected by the time of exposure to ENR. Despite the wide use of ENR to stimulate neuroplasticity, the degree to which ENR variations modeled by temporally changing the level of environmental complexity affect hippocampal neurogenesis and anxiety is still unclear. Thus, we investigated the effects of five housing conditions on young adult male Balb/C mice exposed for 42 days. The groups were as follows standard conditions without ENR, constant ENR complexity, gradual increase of ENR complexity followed by a gradual decrease of ENR complexity, gradual increase of ENR complexity followed by constant ENR complexity, and constant ENR complexity followed by a gradual decrease of ENR complexity. On day 44, mice were exposed to the elevated plus-maze to evaluate anxiety. Further, we analyzed neurogenesis and quantified corticosterone levels. In an additional experiment, we explored the effect of voluntary physical activity on anxiety, neurogenesis, and corticosterone during the variations in ENR complexity. Our results showed that any change in ENR complexity over time reduced anxiety. Also, voluntary physical activity alone or in the context of a complex environment increased doublecortin cell maturation in the granular cell layer of the hippocampus. Finally, our study supports that physical activity acts proneurogenic, whereas any change in environmental complexity decreases anxiety-like behavior. However, the decrease in corticosterone levels elicited by physical activity was lower than the decrease produced by the decrement in environmental complexity.Low-protein diets can impact food intake and appetite, but it is not known if motivation for food is changed. DL-Buthionine-Sulfoximine ic50 In the present study, we used an operant behavioral task - the progressive ratio test - to assess whether motivation for different foods was affected when rats were maintained on a protein-restricted diet (REST, 5% protein diet) compared to non-restricted control rats (CON, 18% protein). Rats were tested either with nutritionally-balanced pellets (18.7% protein, Experiment 1) or protein-rich pellets (35% protein, Experiment 2) as reinforcers. Protein restriction increased breakpoint for protein-rich pellets, relative to CON rats, whereas no difference in breakpoint for nutritionally-balanced pellets was observed between groups. When given free access to either nutritionally-balanced pellets or protein-rich pellets, REST and CON rats did not differ in their intake. We also tested whether a previous history of protein restriction might affect present motivation for different types of food by assessing breakpoint of previously REST animals that were subsequently put on standard maintenance chow (protein-repleted rats, REPL, Experiment 2). REPL rats did not show increased breakpoint, relative to their initial encounter with protein-rich pellets while they were protein-restricted. This study demonstrates that restriction of dietary protein induces a selective increased motivation for protein-rich food, a behavior that disappears once rats are not in need of protein.Adolescence is a period of transition during which there is extensive development of the brain and the hypothalamic-pituitary-adrenal axis. However, the term adolescence is broad and covers a number of important developmental periods ranging from pre-pubescence to sexual maturity. Using a predator stress model, we investigated the effects of chronic psychological stress on anxiety-like, depression-like, and social behaviours in male and female mice during early adolescence, when mice are pre-pubertal, and late adolescence, when mice are sexually mature. All stressed mice showed hyperactivity and increased anxiety-like behaviours. The anxiogenic effects were generally more pronounced in mice exposed to late, rather than early adolescent stress, but were clearly evident when stress was experienced at either timepoint. Risk assessment behaviours were also affected by the stress treatments, but the direction of these changes were sometimes sex- and age-specific. Surprisingly, mice stressed during adolescence showed no depressive-like behaviours as adults. This study provides evidence that adolescent psychological stress has pronounced long-term anxiogenic effects but that the precise behavioural phenotype differs based on sex and the sub-stage of adolescence during which the individual is exposed.Plastic wastes buried in landfill are gradually broken and decomposed into microplastics under physical, chemical and biological effects, bringing environmental risks to the exploitation of waste resources. Landfill leachate as a potential source of environmental microplastics has not good attention. Microplastics in leachate carry toxic and harmful pollutants and antibiotic resistance genes, and these vectors pose greater risks to human and environmental health without systematic treatment. Recently, the main technologies of landfill leachate treatment process include order batch activated sludge process, membrane biological reaction process, flocculation process, combined filtration process, and constructed wetland process. However, there is still little knowledge about microplastic removal of the existing leachate treatment facilities, and some technologies to alleviate the sources of such microplastics should be timely developed. This paper systematically summarizes the occurrence of plastics, microplastics and nanoplastics in leachate and their interactive pollution with other toxic pollutants. Meanwhile, the prospects of their environmental behaviors in landfill and leachate are put forward. The microplastic removal by existing leachate treatment equipment and the limitations and challenges to upgrading process of development and implementation are also discussed. The paper can provide a scientific basis for studying the fate of microplastics in landfill and leachate.The gas-liquid mass transfer rate of hydrophobic volatile organic compounds (VOCs) is the limiting step in a biological treatment system. The present study aimed to utilize self-producing biosurfactants to enhance the bioavailability of hydrophobic gaseous VOCs. Two novel gram-negative rod-shaped bacteria, Enterobacter cloacae strain HN01 and Klebsiella pneumoniae strain HN02 were successfully isolated from sewage sludge by using blood agar and methylene blue agar plates. The two strains can use para-xylene (PX), a hydrophobic VOC model, as the only carbon source for biosurfactant production. Both strains can produce glycolipid biosurfactants, as confirmed by the emulsification index, Nuclear magnetic resonance, and Fourier transform infrared spectroscopy. Results indicated that PX can be completely decomposed at an initial concentration of 15.50 mg L-1, pH value of 7.0, and temperature of 30 °C within 36 h. The Yano model is suitable for the prediction of the growth kinetics of strains over the entire PX concentration range. Gas chromatography/mass spectrometry analysis indicated that PX was converted into four and four intermediates in the presence of the strains HN01 and HN02, respectively, and the possible mechanisms were proposed. The results can be used in purifying industrial hydrophobic gaseous VOCs and improving the bioavailability of VOCs with self-produced biosurfactants.There is an increased awareness that the use of animals for compound-induced developmental neurotoxicity (DNT) testing has limitations. Animal-free innovations, especially the ones based on human stem cell-based models are pivotal in studying DNT since they can mimic processes relevant to human brain development. Here we present the human neural progenitor test (hNPT), a 10-day protocol in which neural progenitor cells differentiate into a neuron-astrocyte co-culture. The study aimed to characterise differentiation over time and to find neurodevelopmental processes sensitive to compound exposure using transcriptomics. 3992 genes regulated in unexposed control cultures (p ≤ 0.001, log2FC ≥ 1) showed Gene Ontology (GO-) term enrichment for neuronal and glial differentiation, neurite extension, synaptogenesis, and synaptic transmission. Exposure to known or suspected DNT compounds (acrylamide, chlorpyrifos, fluoxetine, methyl mercury, or valproic acid) at concentrations resulting in 95% cell viability each regulated unique combinations of GO-terms relating to neural progenitor proliferation, neuronal and glial differentiation, axon development, synaptogenesis, synaptic transmission, and apoptosis.
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