Biomedical subjects

Qing-Guo Ruan

Publications and source records attributed to Qing-Guo Ruan.

3 recordsLinked to original sources

PubMed2004

Autoimmune polyglandular syndrome type 1 and the autoimmune regulator.

The autoimmune polyglandular syndrome type I (APSI) is an auto-somal recessive disorder that is characterized by chronic mucocutaneous candidiasis, multiple autoimmune endocrinopathies, and ectodermal dystrophies. The gene that is responsible for APSI has been identified as autoimmune regulator (AIRE). More than 50 different mutations have been discovered in patients who have APSI and the defects include nonsense and missense mutations, small insertions and deletions that lead to frameshift, and splice site mutations. The 545-amino acid protein that is encoded by AIRE contains several structural motifs that are suggestive of a transcriptional regulator. We provide an overview of the clinical and genetic features ofAPSI as well as the structure and functions of the AIRE protein.

Humans↗

PubMed2004

Molecular pathways altered by insulin b9-23 immunization.

Type 1 diabetes (T1D) in the nonobese diabetic (NOD) mouse can be delayed by administration of insulin or specific insulin peptides. To better understand how insulin treatment delays diabetes development, NOD mice treated with an insulin peptide (B9-23) were compared with age-matched NOD and NOD congenic mice for gene expression changes in spleen using cDNA microarray. Fifty genes were identified that were significantly altered by B9-23 treatment. Thirty-three of these genes are downregulated by the treatment while they are upregulated during the natural disease progression in NOD from immature (3-4 weeks) to mature (10 weeks) stages. Taken together, our data suggest that the B9-23 treatment, like the protective genes in NOD congenic strains, reduces pro-inflammatory activation of lymphocytes that normally occurs in NOD mice. Furthermore, our studies discovered two genes (Irf4 and Tra1) with increased expression in B9-23-treated mice that promote the Th2 response, providing a molecular basis for the B9-23-protective therapy.

Animals↗

PubMed2003

Microarray analysis of gene expression in the kidneys of new- and post-onset diabetic NOD mice.

We profiled the expression of 5,760 clones from a kidney subtraction library in the kidneys of three groups of NOD mice: nondiabetic, new-onset, and long-term diabetic. A total of 27 genes had lower expression and 1 gene (Gpx3) had higher expression in the new-onset diabetic mice compared with nondiabetic control NOD mice (P < 0.001). Similarly, 19 of the above 27 genes and 7 additional genes had higher expression and the Gpx3 gene had lower expression in long-term diabetic mice compared with controls (P < 0.001). Interestingly, only three genes may be different between new-onset and long-term diabetic mice (P < 0.0004). These genes are from diverse functional groups, including oxidative phosphorylation, free radical neutralization, channels, pumps, lipid processing, transcription and translation machinery, protein trafficking, constitutive protein processing, and immune function. The majority of these genes fall into four signaling pathways: insulin, transforming growth factor-beta, tumor necrosis factor-alpha, and peroxisome proliferator-activated receptor. The most significant expression change was found for the stearoyl-coenzyme A desaturase 1 (SCD1) gene (P < 10(-7)). The lower expression levels of the SCD1 gene in both diabetic groups compared with controls were further confirmed by Northern blot analysis and immunohistochemistry.

Animals↗