Table_1_Pathological mechanisms of type 1 diabetes in children: investigation of the exosomal protein expression profile.xlsx

IntroductionType 1 diabetes (T1D) is a serious autoimmune disease with high morbidity and mortality. Early diagnosis and treatment remain unsatisfactory. While the potential for development of T1D biomarkers in circulating exosomes has attracted interest, progress has been limited. This study endeavors to explore the molecular dynamics of plasma exosome proteins in pediatric T1D patients and potential mechanisms correlated with T1D progressionMethodsLiquid chromatography-tandem mass spectrometry with tandem mass tag (TMT)6 labeling was used to quantify exosomal protein expression profiles in 12 healthy controls and 24 T1D patients stratified by age (≤ 6 years old and > 6 years old) and glycated hemoglobin (HbA1c) levels (> 7% or > 7%). Integrated bioinformatics analysis was employed to decipher the functions of differentially expressed proteins, and Western blotting was used for validation of selected proteins' expression levels. ResultsWe identified 1035 differentially expressed proteins (fold change > 1.3) between the T1D patients and healthy controls: 558 in those ≤ 6-year-old and 588 in those > 6-year-old. In those who reached an HbA1c level DiscussionThis study delivers valuable insights into the fundamental molecular mechanisms contributing to T1D pathology. Moreover, it proposes potential therapeutic targets for improved T1D management.</p

Image_3_Pathological mechanisms of type 1 diabetes in children: investigation of the exosomal protein expression profile.jpeg

IntroductionType 1 diabetes (T1D) is a serious autoimmune disease with high morbidity and mortality. Early diagnosis and treatment remain unsatisfactory. While the potential for development of T1D biomarkers in circulating exosomes has attracted interest, progress has been limited. This study endeavors to explore the molecular dynamics of plasma exosome proteins in pediatric T1D patients and potential mechanisms correlated with T1D progressionMethodsLiquid chromatography-tandem mass spectrometry with tandem mass tag (TMT)6 labeling was used to quantify exosomal protein expression profiles in 12 healthy controls and 24 T1D patients stratified by age (≤ 6 years old and > 6 years old) and glycated hemoglobin (HbA1c) levels (> 7% or > 7%). Integrated bioinformatics analysis was employed to decipher the functions of differentially expressed proteins, and Western blotting was used for validation of selected proteins' expression levels. ResultsWe identified 1035 differentially expressed proteins (fold change > 1.3) between the T1D patients and healthy controls: 558 in those ≤ 6-year-old and 588 in those > 6-year-old. In those who reached an HbA1c level DiscussionThis study delivers valuable insights into the fundamental molecular mechanisms contributing to T1D pathology. Moreover, it proposes potential therapeutic targets for improved T1D management.</p

Image_2_Pathological mechanisms of type 1 diabetes in children: investigation of the exosomal protein expression profile.jpeg

IntroductionType 1 diabetes (T1D) is a serious autoimmune disease with high morbidity and mortality. Early diagnosis and treatment remain unsatisfactory. While the potential for development of T1D biomarkers in circulating exosomes has attracted interest, progress has been limited. This study endeavors to explore the molecular dynamics of plasma exosome proteins in pediatric T1D patients and potential mechanisms correlated with T1D progressionMethodsLiquid chromatography-tandem mass spectrometry with tandem mass tag (TMT)6 labeling was used to quantify exosomal protein expression profiles in 12 healthy controls and 24 T1D patients stratified by age (≤ 6 years old and > 6 years old) and glycated hemoglobin (HbA1c) levels (> 7% or > 7%). Integrated bioinformatics analysis was employed to decipher the functions of differentially expressed proteins, and Western blotting was used for validation of selected proteins' expression levels. ResultsWe identified 1035 differentially expressed proteins (fold change > 1.3) between the T1D patients and healthy controls: 558 in those ≤ 6-year-old and 588 in those > 6-year-old. In those who reached an HbA1c level DiscussionThis study delivers valuable insights into the fundamental molecular mechanisms contributing to T1D pathology. Moreover, it proposes potential therapeutic targets for improved T1D management.</p

Image_5_Pathological mechanisms of type 1 diabetes in children: investigation of the exosomal protein expression profile.pdf

IntroductionType 1 diabetes (T1D) is a serious autoimmune disease with high morbidity and mortality. Early diagnosis and treatment remain unsatisfactory. While the potential for development of T1D biomarkers in circulating exosomes has attracted interest, progress has been limited. This study endeavors to explore the molecular dynamics of plasma exosome proteins in pediatric T1D patients and potential mechanisms correlated with T1D progressionMethodsLiquid chromatography-tandem mass spectrometry with tandem mass tag (TMT)6 labeling was used to quantify exosomal protein expression profiles in 12 healthy controls and 24 T1D patients stratified by age (≤ 6 years old and > 6 years old) and glycated hemoglobin (HbA1c) levels (> 7% or > 7%). Integrated bioinformatics analysis was employed to decipher the functions of differentially expressed proteins, and Western blotting was used for validation of selected proteins' expression levels. ResultsWe identified 1035 differentially expressed proteins (fold change > 1.3) between the T1D patients and healthy controls: 558 in those ≤ 6-year-old and 588 in those > 6-year-old. In those who reached an HbA1c level DiscussionThis study delivers valuable insights into the fundamental molecular mechanisms contributing to T1D pathology. Moreover, it proposes potential therapeutic targets for improved T1D management.</p

Image_4_Pathological mechanisms of type 1 diabetes in children: investigation of the exosomal protein expression profile.jpeg

IntroductionType 1 diabetes (T1D) is a serious autoimmune disease with high morbidity and mortality. Early diagnosis and treatment remain unsatisfactory. While the potential for development of T1D biomarkers in circulating exosomes has attracted interest, progress has been limited. This study endeavors to explore the molecular dynamics of plasma exosome proteins in pediatric T1D patients and potential mechanisms correlated with T1D progressionMethodsLiquid chromatography-tandem mass spectrometry with tandem mass tag (TMT)6 labeling was used to quantify exosomal protein expression profiles in 12 healthy controls and 24 T1D patients stratified by age (≤ 6 years old and > 6 years old) and glycated hemoglobin (HbA1c) levels (> 7% or > 7%). Integrated bioinformatics analysis was employed to decipher the functions of differentially expressed proteins, and Western blotting was used for validation of selected proteins' expression levels. ResultsWe identified 1035 differentially expressed proteins (fold change > 1.3) between the T1D patients and healthy controls: 558 in those ≤ 6-year-old and 588 in those > 6-year-old. In those who reached an HbA1c level DiscussionThis study delivers valuable insights into the fundamental molecular mechanisms contributing to T1D pathology. Moreover, it proposes potential therapeutic targets for improved T1D management.</p

Image_1_Pathological mechanisms of type 1 diabetes in children: investigation of the exosomal protein expression profile.jpeg

IntroductionType 1 diabetes (T1D) is a serious autoimmune disease with high morbidity and mortality. Early diagnosis and treatment remain unsatisfactory. While the potential for development of T1D biomarkers in circulating exosomes has attracted interest, progress has been limited. This study endeavors to explore the molecular dynamics of plasma exosome proteins in pediatric T1D patients and potential mechanisms correlated with T1D progressionMethodsLiquid chromatography-tandem mass spectrometry with tandem mass tag (TMT)6 labeling was used to quantify exosomal protein expression profiles in 12 healthy controls and 24 T1D patients stratified by age (≤ 6 years old and > 6 years old) and glycated hemoglobin (HbA1c) levels (> 7% or > 7%). Integrated bioinformatics analysis was employed to decipher the functions of differentially expressed proteins, and Western blotting was used for validation of selected proteins' expression levels. ResultsWe identified 1035 differentially expressed proteins (fold change > 1.3) between the T1D patients and healthy controls: 558 in those ≤ 6-year-old and 588 in those > 6-year-old. In those who reached an HbA1c level DiscussionThis study delivers valuable insights into the fundamental molecular mechanisms contributing to T1D pathology. Moreover, it proposes potential therapeutic targets for improved T1D management.</p

Additional file 1 of Plasma metabolomic profile in orthostatic intolerance children with high levels of plasma homocysteine

Supplementary Material: Table S1. Significantly differential metabolite

Wide ectopic mRNA levels of imprinted genes in mouse fetuses with RA-induced spina bifida.

<p>(<b>A and B</b>) The real-time qPCR assay results indicate the fold change in imprinted genes on each chromosome in the spinal cord tissue of E18 RA-induced mice with NTDs compared with control. The x-axis represents the chromosome and the relative genomic position of each gene. The y-axis represents the relative mRNA abundance in NTDs compared with the control. The red column indicates a maternally expressed gene, while the blue column indicates a paternally expressed gene. *: <i>P</i><0.05; **: <i>P</i><0.01; ***: <i>P</i><0.0001 (Student's <i>t</i>-test).</p

Hypermethylated <i>H19</i> DMR1 and stably methylated <i>IGF2</i> DMR0 in human fetuses with NTDs.

<p>The DNA methylation levels of the <i>H19</i> DMR1 (A) and <i>IGF2</i> DMR0 (B) were examined through matrix-assisted laser desorption/ionization time-of-flight (MALDI-TOF) mass spectrometry. In the upper panel in (A) and right panel in (B), the methylation status of all detected CpG sites was visualized. Each solid circle represents a “CG” site. (A)The number in upper panel refers to the CG site(s) in the lower histogram. (B) The number in the left panel refers to the site in the right histogram. ***: <i>P</i><0.0001 (Student's <i>t</i>-test).</p

More open chromatin structure in mice fetuses with RA-induced spina bifida.

<p>(A) The methylation level of <i>H19</i> DMR1 is stable in RA-treated mice. For details, see the legend in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0113308#pone-0113308-g003" target="_blank">Fig. 3</a>. (B) and (F): The genomic profile of genes displayed in UCSC (mm9), the genomic locus of target regions in ChIP assay (black block in the gene schematic) (corresponding results shown in C and D or G and H), and the CpG island (green block underneath the gene schematic) (corresponding results shown in E and I) detected by MASSARRAY assay are shown. The number beside the block indicates the genomic location that was targeted. In the ChIP assay results (C and D or G and H), the enrichment in the y-axis represents the relative fold enrichment in which the higher enrichment in case or control is designated as 1. *: <i>P</i><0.05; **: <i>P</i><0.01; ***: <i>P</i><0.0001 (Student's <i>t</i>-test). TSS: transcription start site.</p