37 research outputs found

    Individuals with Eating Disorder Symptoms Have an Increased Risk of Nightmares

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    Objective: This preliminary study was aimed to examine if individuals with eating disorder symptoms have a higher incidence of nightmares. Additionally, the possible influence of general psychological distress on the relationship between eating disorder symptoms and nightmares was examined.Methods: Using a cross-sectional design, 350 university students completed measurements of nightmare frequency, eating disorder symptoms, and psychological distress.Results: Individuals reporting symptoms of eating disorders were significantly more likely to report frequent nightmares compared to controls. However, when controlling for gender and general psychological distress, eating disorder symptomatology no longer significantly predicted nightmares.Conclusion: Individuals reporting symptoms of eating disorders are more likely to report nightmares. However, the incidence of nightmares among individuals with eating disorder symptoms appears to be largely affected by gender and levels of general distress. Further research is suggested to extend and replicate these preliminary results among clinical samples. Physicians with patients reporting eating disorder symptoms should consider screening for the presence of nightmares

    AllSpark: A Multimodal Spatio-Temporal General Intelligence Model with Thirteen Modalities

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    For a long time, due to the high heterogeneity in structure and semantics among various spatiotemporal modal data, the joint interpretation of multimodal spatiotemporal data has been an extremely challenging problem. The primary challenge resides in striking a trade-off between the cohesion and autonomy of diverse modalities, and this trade-off exhibits a progressively nonlinear nature as the number of modalities expands. We introduce the Language as Reference Framework (LaRF), a fundamental principle for constructing a multimodal unified model, aiming to strike a trade-off between the cohesion and autonomy among different modalities. We propose a multimodal spatiotemporal general artificial intelligence model, called AllSpark. Our model integrates thirteen different modalities into a unified framework, including 1D (text, code), 2D (RGB, infrared, SAR, multispectral, hyperspectral, tables, graphs, trajectory, oblique photography), and 3D (point clouds, videos) modalities. To achieve modal cohesion, AllSpark uniformly maps diverse modal features to the language modality. In addition, we design modality-specific prompts to guide multi-modal large language models in accurately perceiving multimodal data. To maintain modality autonomy, AllSpark introduces modality-specific encoders to extract the tokens of various spatiotemporal modalities. And modal bridge is employed to achieve dimensional projection from each modality to the language modality. Finally, observing a gap between the model's interpretation and downstream tasks, we designed task heads to enhance the model's generalization capability on specific downstream tasks. Experiments indicate that AllSpark achieves competitive accuracy in modalities such as RGB and trajectory compared to state-of-the-art models.Comment: 49 pages, 16 tables, 3 figure

    Young plasma reverses anesthesia and surgery-induced cognitive impairment in aged rats by modulating hippocampal synaptic plasticity

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    We investigated the protective effect of young plasma on anesthesia- and surgery-induced cognitive impairment and the potential underlying mechanism using bioinformatics, functional enrichment analysis, gene set enrichment analysis, Golgi-Cox staining, dendritic spine analysis, immunofluorescence assay, western blot analysis, and transmission electron microscopy. Furthermore, we performed behavioral assessments using the open field test, the novel object recognition test, and the Morris water maze test. We identified 1969 differentially expressed genes induced by young plasma treatment, including 800 upregulated genes and 1169 downregulated genes, highlighting several enriched biological processes (signal release from synapse, postsynaptic density and neuron to neuron synapse). Anesthesia- and surgery-induced cognitive impairment in aged rats was comparatively less severe following young plasma preinfusion. In addition, the decreased levels of synapse-related and tyrosine kinase B/extracellular signal-regulated protein kinase/cyclic adenosine monophosphate response element-binding protein (TrkB/ERK/CREB) signaling pathway-related proteins, dendritic and spine deficits, and ultrastructural changes were ameliorated in aged mice following young plasma preinfusion. Together, these findings suggest that young plasma reverses anesthesia- and surgery-induced cognitive impairment in aged rats and that the mechanism is associated with the activation of the TrkB/ERK/CREB signaling pathway and improvement in hippocampal synaptic plasticity

    Frataxin deficiency promotes endothelial senescence in pulmonary hypertension

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    The dynamic regulation of endothelial pathophenotypes in pulmonary hypertension (PH) remains undefined. Cellular senescence is linked to PH with intracardiac shunts; however, its regulation across PH subtypes is unknown. Since endothelial deficiency of iron-sulfur (Fe-S) clusters is pathogenic in PH, we hypothesized that a Fe-S biogenesis protein, frataxin (FXN), controls endothelial senescence. An endothelial subpopulation in rodent and patient lungs across PH subtypes exhibited reduced FXN and elevated senescence. In vitro, hypoxic and inflammatory FXN deficiency abrogated activity of endothelial Fe-S–containing polymerases, promoting replication stress, DNA damage response, and senescence. This was also observed in stem cell–derived endothelial cells from Friedreich’s ataxia (FRDA), a genetic disease of FXN deficiency, ataxia, and cardiomyopathy, often with PH. In vivo, FXN deficiency–dependent senescence drove vessel inflammation, remodeling, and PH, whereas pharmacologic removal of senescent cells in Fxn-deficient rodents ameliorated PH. These data offer a model of endothelial biology in PH, where FXN deficiency generates a senescent endothelial subpopulation, promoting vascular inflammatory and proliferative signals in other cells to drive disease. These findings also establish an endothelial etiology for PH in FRDA and left heart disease and support therapeutic development of senolytic drugs, reversing effects of Fe-S deficiency across PH subtypes

    Inhibition of MicroRNA-383 Ameliorates Injury After Focal Cerebral Ischemia via Targeting PPARγ

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    Background: Peroxisome proliferator-activated receptor gamma (PPARγ) plays a critical role in protecting against distinct brain damages, including ischemia. Our previous data have shown that the protein level of PPARγ is increased in the cortex after middle cerebral artery occlusion (MCAO); PPARγ up-regulation contributes to PPARγ activation and is effective in reducing ischemic damage to brain. However, the regulatory mechanism of PPARγ after focal cerebral ischemia in rats is still unclear. In this study, we evaluated the effect of microRNA on PPARγ in rats subjected to MCAO. Methods: Focal cerebral ischemia was established by surgical middle cerebral artery occlusion; the protein level of PPARγ was detected by Western blotting; the level of microRNA-383 (miR-383) was quantified by real-time PCR; the neurological outcomes were defined by infarct volume and neurological deficits. Luciferase assay was used to identify the luciferase activities of PPARγ and miR-383. Results: We showed here that miR-383 level was down-regulated in the ischemic hemisphere of rats 24h after MCAO. Overexpression of miR-383 by miR-383 agomir increased infarct volume and aggravated neurological damage. Administration of miR-383 antagomir had the opposite effects. Furthermore, we found that PPARγ protein was down-regulated by miR-383 overexpression, and up-regulated by miR-383 inhibition both in rat model of MCAO and in primary culture cells. Finally, we found that miR-383 suppressed the luciferase activity of the vector carrying the 3'UTR of PPARγ, whereas mutation of the binding sites relived the repressive effect of miR-383. Conclusion: Our study demonstrated that miR-383 may play a key role in focal cerebral ischemia by regulating PPARγ expression at the post-transcriptional level, and miR-383 may be a potential therapeutic target for stroke

    Effects of exogenous salicylic acid on accumulation of camptothecin and gene expression in Camptotheca acuminata Decne

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    Camptotheca acuminata Decne (Nyssaceae) is major natural source of camptothecin, an anticancer drug widely used for clinic therapy. Previous works have shown that many plant hormones/elicitors could regulate camptothecin biosynthesis, but few reports have examined sustanable effects of these plant hormones on plants for producing camptothecin. In this work, seedlings obtained from in vitro rapid propagation were used for investigating sustainable effect of Salicylic acid (SA) on transplanted C. acuminata tissues, especially leaves, for camptothecin biosynthesis. Our results indicate that exogenous SA could continuously induce the expression of iridoids pathway genes in C. acuminata leaves for promoting camptothecin production. After transplanted to soil for 180 days, high expression of iridoids pathway genes still could be observed in bioactive young leaves. In C. acuminata, iridoids pathway genes are expressed at very low levels or not detectable in old leaves, which lead to inefficient production of camptothecin with leaf development. Interestingly, the expression of these genes could be clearly detected in old leaves of transplanted C. acuminata pretreated with 10 ÂľM of SA during in vitro rapid propagation phase, which indicates particular function of SA for sustainable effect on maintaining relative high expression levels of iridoids pathway genes for camptothecin biosynthesis.The accepted manuscript in pdf format is listed with the files at the bottom of this page. The presentation of the authors' names and (or) special characters in the title of the manuscript may differ slightly between what is listed on this page and what is listed in the pdf file of the accepted manuscript; that in the pdf file of the accepted manuscript is what was submitted by the author
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