37 research outputs found

    RENAL ISCHEMIA REPERFUSION CAUSES BRAIN HIPPOCAMPUS OXIDATIVE DAMAGE AND INHIBITION EFFECT

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    Background: The acute kidney injury (AKI) may do damage to remote organs. Objective of the study is to investigate effect of seaweed extract (SE) on brain oxidative damage in kidney ischemia/reperfusion rats. Material and Methods: Animals were randomly divided into five groups. SE pre-fed to rats. Results: Kidney I/R may cause oxidative injury in kidneys and brains tissue in rats. SE pre-treatment can decrease lipid peroxidation levels and increase antioxidant enzymes activities in kidney and brain hippocampus of kidney I/R rats. Conclusion: Our results indicate that SE is useful for brain nerve function keeping in kidney I/R rats

    INHIBITION OF PACLITAXEL AGAINST NEUROGLIOMA CELLS U251 GROWTH AND ITS MECHANISM

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    Background: Glioma is the most common primary tumor of the central nervous system, and accounted for about 70% of primary tumors. Materials and Methods: In the study, antitumour activity and mechanism of paclitaxel was investigated. Different concentrations of paclitaxel (200, 300, 400 ÎĽmol/L) was treated in neuroglioma cellsU251. Results: Paclitaxel significantly inhibited neuroglioma cells growth, and promoted its apoptosis. Paclitaxel can block tumour cells in the G2/M phase. In addition, apoptosis-related genes caspase-3 and bax expressions were increased after paclitaxel treatment. Conclusion: Our work indicated that paclitaxel displayed strong anti-tumour activity

    Neurological Diseases With Autism Spectrum Disorder: Role of ASD Risk Genes

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    Autism spectrum disorder (ASD) is frequently comorbid with other neurological disorders such as intellectual disability (ID) or global development delay (GDD) and epilepsy. The pathogenesis of ASD is complex. So far, studies have identified more than 1000 ASD risk genes. Most of them were also reported to relate with other neurological diseases, and only several of them have been confirmed as pathogenic genes for autism. Little is known about the roles of these risk genes in neurological diseases with ASD. In the present study, we recruited a cohort of 158 neurological disorder probands with 163 variants of 48 ASD risk genes. Of these, 50 individuals (31.6%) were diagnosed with ASD. In the ASD patient subset, we identified several rarely reported candidate genes including DOLK, USH2A, and HUWE1. In a comparison of patients with neurological disorders with and without ASD, we found that ID/GDD was frequently comorbid with ASD whereas epilepsy was more common in the non-ASD group. Statistical analyses of all possible risk factors implicated that variants in synaptic genes, especially non-voltage-gated ion channel genes and in transcriptional and chromosome genes were related to ASD, but none of the investigated environmental factors was. Our results are useful for the future diagnosis and prognosis of patients with neurological disorders and emphasize the utility of genetic screening

    A Low-Cost and Portable Dual-Channel Fiber Optic Surface Plasmon Resonance System

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    A miniaturization and integration dual-channel fiber optic surface plasmon resonance (SPR) system was proposed and demonstrated in this paper. We used a yellow light-emitting diode (LED, peak wavelength 595 nm) and built-in web camera as a light source and detector, respectively. Except for the detection channel, one of the sensors was used as a reference channel to compensate nonspecific binding and physical absorption. We packaged the LED and surface plasmon resonance (SPR) sensors together, which are flexible enough to be applied to mobile devices as a compact and portable system. Experimental results show that the normalized intensity shift and refractive index (RI) of the sample have a good linear relationship in the RI range from 1.328 to 1.348. We used this sensor to monitor the reversible, specific interaction between lectin concanavalin A (Con A) and glycoprotein ribonuclease B (RNase B), which demonstrate its capabilities of specific identification and biochemical samples concentration detection. This sensor system has potential applications in various fields, such as medical diagnosis, public health, food safety, and environment monitoring

    Contralesional Cortical and Network Features Associated with Preoperative Language Deficit in Glioma Patients

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    Lower-grade Gliomas anchored in eloquent areas cause varying degrees of language impairment. Except for a tumor’s features, contralesional compensation may explain these differences. Therefore, studying changes in the contralateral hemisphere can provide insights into the underlying mechanisms of language function compensation in patients with gliomas. This study included 60 patients with eloquent-area or near-eloquent-area gliomas. The participants were grouped according to the degree of language defect. T1 and diffusion tensor imaging were obtained. The contralesional cortical volume and the subcortical network were compared between groups. Patients with unimpaired language function showed elevated cortical volume in the midline areas of the frontal and temporal lobes. In subcortical networks, the group also had the highest global efficiency and shortest global path length. Ten nodes had intergroup differences in nodal efficiency, among which four nodes were in the motor area and four nodes were in the language area. Linear correlation was observed between the efficiency of the two nodes and the patient’s language function score. Functional compensation in the contralesional hemisphere may alleviate language deficits in patients with gliomas. Structural compensation mainly occurs in the contralesional midline area in the frontal and temporal lobes, and manifests as an increase in cortical volume and subcortical network efficiency

    First-Principles Calculations of the Mechanical Properties of Doped Cu<sub>3</sub>P Alloys

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    In the quest to enhance the mechanical properties of CuP alloys, particularly focusing on the Cu3P phase, this study introduces a comprehensive investigation into the effects of various alloying elements on the alloy’s performance. In this paper, the first principle of density universal function theory and the projection-enhanced wave method under VASP 5.4.4 software are used to recalculate the lattice constants, evaluate the lattice stability, and explore the mechanical properties of selected doped elements such as In, Si, V, Al, Bi, Nb, Sc, Ta, Ti, Y and Zr, including shear, stiffness, compression, and plasticity. The investigation reveals that strategic doping with In and Si significantly enhances shear resistance and stiffness, while V addition notably augments compressive resistance. Furthermore, incorporating Al, Bi, Nb, Sc, Ta, Ti, V, Y, and Zr has substantially improved plasticity, indicating a broad spectrum of mechanical enhancement through precise alloying. Crucially, the validation of our computational models is demonstrated through hardness experiments on Si and Sn-doped specimens, corroborating the theoretical predictions. Additionally, a meticulous analysis of the states’ density further confirms our computational approach’s accuracy and reliability. This study highlights the potential of targeted alloying to tailor the mechanical properties of Cu3P alloys and establishes a robust theoretical framework for predicting the effects of doping in metallic alloys. The findings presented herein offer valuable insights and a novel perspective on material design and optimization, marking a significant stride toward developing advanced materials with customized mechanical properties

    Data_Sheet_1_Identification of potential drug targets for insomnia by Mendelian randomization analysis based on plasma proteomics.DOCX

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    IntroductionInsomnia, a common clinical disorder, significantly impacts the physical and mental well-being of patients. Currently, available hypnotic medications are unsatisfactory due to adverse reactions and dependency, necessitating the identification of new drug targets for the treatment of insomnia.MethodsIn this study, we utilized 734 plasma proteins as genetic instruments obtained from genome-wide association studies to conduct a Mendelian randomization analysis, with insomnia as the outcome variable, to identify potential drug targets for insomnia. Additionally, we validated our results externally using other datasets. Sensitivity analyses entailed reverse Mendelian randomization analysis, Bayesian co-localization analysis, and phenotype scanning. Furthermore, we constructed a protein-protein interaction network to elucidate potential correlations between the identified proteins and existing targets.ResultsMendelian randomization analysis indicated that elevated levels of TGFBI (OR = 1.01; 95% CI, 1.01–1.02) and PAM ((OR = 1.01; 95% CI, 1.01–1.02) in plasma are associated with an increased risk of insomnia, with external validation supporting these findings. Moreover, there was no evidence of reverse causality for these two proteins. Co-localization analysis confirmed that PAM (coloc.abf-PPH4 = 0.823) shared the same variant with insomnia, further substantiating its potential role as a therapeutic target. There are interactive relationships between the potential proteins and existing targets of insomnia.ConclusionOverall, our findings suggested that elevated plasma levels of TGFBI and PAM are connected with an increased risk of insomnia and might be promising therapeutic targets, particularly PAM. However, further exploration is necessary to fully understand the underlying mechanisms involved.</p

    Data_Sheet_2_Identification of potential drug targets for insomnia by Mendelian randomization analysis based on plasma proteomics.XLSX

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    IntroductionInsomnia, a common clinical disorder, significantly impacts the physical and mental well-being of patients. Currently, available hypnotic medications are unsatisfactory due to adverse reactions and dependency, necessitating the identification of new drug targets for the treatment of insomnia.MethodsIn this study, we utilized 734 plasma proteins as genetic instruments obtained from genome-wide association studies to conduct a Mendelian randomization analysis, with insomnia as the outcome variable, to identify potential drug targets for insomnia. Additionally, we validated our results externally using other datasets. Sensitivity analyses entailed reverse Mendelian randomization analysis, Bayesian co-localization analysis, and phenotype scanning. Furthermore, we constructed a protein-protein interaction network to elucidate potential correlations between the identified proteins and existing targets.ResultsMendelian randomization analysis indicated that elevated levels of TGFBI (OR = 1.01; 95% CI, 1.01–1.02) and PAM ((OR = 1.01; 95% CI, 1.01–1.02) in plasma are associated with an increased risk of insomnia, with external validation supporting these findings. Moreover, there was no evidence of reverse causality for these two proteins. Co-localization analysis confirmed that PAM (coloc.abf-PPH4 = 0.823) shared the same variant with insomnia, further substantiating its potential role as a therapeutic target. There are interactive relationships between the potential proteins and existing targets of insomnia.ConclusionOverall, our findings suggested that elevated plasma levels of TGFBI and PAM are connected with an increased risk of insomnia and might be promising therapeutic targets, particularly PAM. However, further exploration is necessary to fully understand the underlying mechanisms involved.</p
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