Proton magnetic resonance spectroscopy provides a non-invasive technology to study brain metabolite levels in vivo, which can be used to measure biochemical compounds or metabolite concentrations in circumscribed brain regions. Previous research has highlighted the role of glial cells in brain white matter. It has been assumed that antidepressant treatment with SSRIs not only affects neurons, but also activates glial cells. This study focused on the observation of any potential changes in the metabolite levels of the ventral prefrontal white matter in major depressive disorder (MDD) patients who have received antidepressant treatment. 17 female patients diagnosed as MDD according to Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV) criteria with the scores of 18 and above on the 24-item Hamilton Depression Rating Scale (HDRS) were recruited. MRS studies were performed on a 3.0 T MR system, single voxel PRESS spectroscopy with chemical-shift selective saturation water suppression. The volume of interest was localized at the bilateral ventral prefrontal white matter regions (voxel size: 2 × 2 × 2 mm3). The spectral data analysis was performed by using the instrument manufacturer supplied software. The bilateral ventral prefrontal white matter of MDD patients showed significantly lower Cho/Cr (p < 0.05) before receiving treatment. The HDRS, as the indicator of treatment response, showed a significant decrease in patients who had gone through 12 weeks treatment (p < 0.01). The bilateral Cho/Cr values of post-treatment patients were increased significantly compared to that of pre-treatment (p < 0.05). The alteration of ventral prefrontal white matter metabolite levels are likely involved in MDD pathophysiology and imply a crucial role of white matter in MDD.

Rheumatoid arthritis (RA) is a systemic disease characterized by non-infectious inflammation of the joints and surrounding tissues, which can cause severe health problems, affect the patient’s daily life, and even cause death. RA can be clinically diagnosed by the occurrence of blood serological markers, rheumatoid factor (RF) and anti-cyclic citrullinated peptide antibody (anti-CCP). However, about 20% of RA patients exhibit negative results for both markers, which makes RA diagnosis difficult and, therefore, may delay the effective treatment. Previous studies found some evidence that human leukocyte antigen (HLA)-related genes might be the susceptibility genes for RA and their polymorphisms might contribute to varieties of susceptibility and disease severity. This study aimed for the genetic polymorphisms of the RA patient genome and their effects on the RA patient’s serological makers, RF and anti-CCP. A total of 4580 patients’ electronic medical records from 1992 to 2020 were retrieved from the China Medical University Hospital database. The most representative single-nucleotide polymorphisms (SNPs) were identified through a genome-wide association study (GWAS) followed by enzyme-linked immunosorbent assay (ELISA) validation using the blood from 30 additional RA patients. The results showed significant changes at the position of chromosome 6 with rs9270481 being the most significant locus, which indicated the location of the HLA-DRB1 gene. Further, patients with the CC genotype at this locus were more likely to exhibit negative results for RF and anti-CCP than those with the TT genotype. The C allele was also more likely to be associated with negative results for RF and anti-CCP. The results demonstrated that a genetic polymorphism at rs9270481 affected the expression of RF and anti-CCP in RA patients, which might indicate the necessity to develop a personalized treatment plan for each individual patient based on the genetic profile.

Major depressive disorder (MDD) frequently co-occurs with other psychiatric problems. Our previous study showed that ATP1A1 gene expression level was significantly decreased in MDD patients. This research explores the potential correlations between the ATP1A1 expression level reduction and MDD patients' clinical manifestation. All participant patients were diagnosed by Diagnostic and Statistical Manual of Mental Disorders - 4th edition (DSM-IV). Hamilton rating scale for depression (HAM-D) and anxiety (HAM-A) were applied to group patients into different categories. ATP1A1 expression level was measured by reverse transcript real-time polymerase chain reaction. ATP1A1 expression levels of all MDD subgroups showed significant reduction compared to the control group (p<0.01). Further, the trend of ATP1A1 expression level reduction is significantly related to MDD patients' HAM-A scores (p0.05). ATP1A1 expression level reduction is related to MDD anxiety score, which may be an explanation for the clinical manifestations and the underlining physiological mechanisms.