Additional file 1 of The low prevalence rate of vitamin E deficiency in urban adults of Wuhan from central China: findings from a single-center, cross-sectional study

Additional file 1: Table S1 Method validation. Table S2 Classification of the subjects according to their TC levels in adults (n=846). Table S3 Classification of the subjects according to their blood pressures in adults (n=846). Table S4 Classification of the subjects according to their BMI in adults (n=846)

DataSheet1_Ontology Specific Alternative Splicing Changes in Alzheimer’s Disease.ZIP

Alternative splicing (AS) is a common phenomenon and correlates with aging and aging-related disorders including Alzheimer’s disease (AD). We aimed to systematically characterize AS changes in the cerebral cortex of 9-month-old APP/PS1 mice. The GSE132177 dataset was downloaded from GEO and ENA databases, aligned to the GRCm39 reference genome from ENSEMBL via STAR. Alternative 3′SS (A3SS), alternative 5′SS (A5SS), skipped exon (SE), retained intron (RI), and mutually exclusive exons (MXE) AS events were evaluated using rMATS, rmats2sashimiplot, and maser. Differential genes or transcripts were analyzed using the limma R package. Gene ontology analysis was performed with the clusterProfiler R package. A total of 60,705 raw counts of AS were identified, and 113 significant AS events were finally selected in accordance with the selection criteria: 1) average coverage >10 and 2) delta percent spliced in (ΔPSI) >0.1. SE was the most abundant AS event (61.95%), and RI was the second most abundant AS type (13.27%), followed by A3SS (12.39%), thereafter A5SS and MXE comprised of 12.39%. Interestingly, genes that experienced SE were enriched in histone acetyltransferase (HAT) complex, while genes spliced by RI were enriched in autophagy and those which experienced A3SS were enriched in methyltransferase activity revealed by GO analysis. In conclusion, we revealed ontology specific AS changes in AD. Our analysis provides novel pathological mechanisms of AD.</p

Additional file 2 of Low-intensity pulsed ultrasound promotes mesenchymal stem cell transplantation-based articular cartilage regeneration via inhibiting the TNF signaling pathway

Additional file 2 Figure S1: Representative Alcian blue staining images for the chondrocyte spheres in suspension culture for LIPUS stimulation and adhered for staining. Figure S2: Western blot data of chondrogenic proteins (COL-II, ACAN, and SOX-9) and actin after different parameters of LIPUS stimulatio

Additional file 3 of Low-intensity pulsed ultrasound promotes mesenchymal stem cell transplantation-based articular cartilage regeneration via inhibiting the TNF signaling pathway

Additional file 3 Full-length blots of the data shown in Figure S2

Additional file 1 of Low-intensity pulsed ultrasound promotes mesenchymal stem cell transplantation-based articular cartilage regeneration via inhibiting the TNF signaling pathway

Additional file 1 Table S1: Lists of hUC-MSCs qPCR primers. Table S2: Lists of C28/I2 qPCR primer

Supplementary document for Nakagami statistics-based photoacoustic spectroscopy used for characterization of molecules in bone tissue - 6183476.pdf

Supplement1, including Sction1-

A flow chart summarizing the study selection process for this meta-analysis.

<p>A flow chart summarizing the study selection process for this meta-analysis.</p

Characteristics of included studies.

<p>Characteristics of included studies.</p

Table_3_Single-cell RNA sequencing of CSF reveals neuroprotective RAC1+ NK cells in Parkinson’s disease.xlsx

Brain infiltration of the natural killer (NK) cells has been observed in several neurodegenerative disorders, including Parkinson’s disease (PD). In a mouse model of α-synucleinopathy, it has been shown that NK cells help in clearing α-synuclein (α-syn) aggregates. This study aimed to investigate the molecular mechanisms underlying the brain infiltration of NK cells in PD. Immunofluorescence assay was performed using the anti-NKp46 antibody to detect NK cells in the brain of PD model mice. Next, we analyzed the publicly available single-cell RNA sequencing (scRNA-seq) data (GSE141578) of the cerebrospinal fluid (CSF) from patients with PD to characterize the CSF immune landscape in PD. Results showed that NK cells infiltrate the substantia nigra (SN) of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced PD model mice and colocalize with dopaminergic neurons and α-syn. Moreover, the ratio of NK cells was found to be increased in the CSF of PD patients. Analysis of the scRNA-seq data revealed that Rac family small GTPase 1 (RAC1) was the most significantly upregulated gene in NK cells from PD patients. Furthermore, genes involved in regulating SN development were enriched in RAC1+ NK cells and these cells showed increased brain infiltration in MPTP-induced PD mice. In conclusion, NK cells actively home to the SN of PD model mice and RAC1 might be involved in regulating this process. Moreover, RAC1+ NK cells play a neuroprotective role in PD.</p

Image_3_Identification of Key eRNAs for Spinal Cord Injury by Integrated Multinomial Bioinformatics Analysis.TIF

Background: Spinal cord injury (SCI) is a severe neurological deficit affecting both young and older people worldwide. The potential role of key enhancer RNAs (eRNAs) in SCI remains elusive, which is a prominent challenge in the trauma repair process. This study aims to investigate the roles of key eRNAs, transcription factors (TFs), signaling pathways, and small-molecule inhibitors in SCI using multi-omics bioinformatics analysis.Methods: Microarray data of peripheral blood mononuclear cell (PBMC) samples from 27 healthy volunteers and 25 chronic-phase SCI patients were retrieved from the Gene Expression Omnibus database. Differentially expressed transcription factors (DETFs), differentially expressed enhancer RNAs (DEeRNAs), and differentially expressed target genes (DETGs) were identified using the Linear Models for Microarray Data (limma) package. Fraction of immune cells was estimated using CIBERSORT algorithm. Gene Set Variation Analysis (GSVA) was applied to identify the downstream signaling pathways. The eRNA regulatory network was constructed based on the correlation results. Connectivity Map (CMap) database was used to find potential drugs for SCI patients. The cellular communication analysis was performed to explore the molecular regulation mechanism of SCI based on single-cell RNA sequencing (scRNA-seq) data. Chromatin immunoprecipitation sequencing (ChIP-seq) and Assay for Transposase-Accessible Chromatin using sequencing (ATAC-seq) data were used to validate the key regulatory mechanisms. scRNA-seq dataset was used to validate the cell subtype localization of the key eRNAs.Results: In total, 21 DETFs, 24 DEeRNAs, and 829 DETGs were identified. A regulatory network of 13 DETFs, six DEeRNAs, seven DETGs, two hallmark pathways, two immune cells, and six immune pathways was constructed. The link of Splicing factor proline and glutamine rich (SFPQ) (TF) and vesicular overexpressed in cancer prosurvival protein 1 (VOPP1) (eRNA) (R = 0.990, p Conclusion: VOPP1, upregulated by SFPQ, strengthened the transient expression of EGFR. Th cells and coagulation were the potential downstream pathways of VOPP1. This regulatory network and potential inhibitors provide novel diagnostic biomarkers and therapeutic targets for SCI.</p