Abstract.Major depressive disorder is a common chronic emotional disorder, and cyclic adenosine monophosphate response element binding protein 1 (CREB1) is hypothesized to play a role in its pathogenesis. The aim of the present study was to investigate the associations between major depressive disorder and relevant single nucleotide polymorphisms (SNPs) in the CREB1 gene. A total of 1,038 subjects of Han Chinese descent were recruited, including 456 patients with major depressive disorder (case group) and 582 healthy volunteers (control group). The frequency distributions of the genotypes and alleles were estimated in the case and control groups, and analyzed for any correlation with major depressive disorder. Three relevant SNP sites in CREB1 were analyzed using quantitative polymerase chain reaction, and statistical analyses were performed to estimate their use as risk factors for major depressive disorder. The analyses revealed that rs2254137 and rs16839883 in CREB1 showed polymorphisms in the sample population, and the genotype and allele frequencies of rs16839883 differed significantly when comparing the patients and healthy controls (P<0.05). No statistically significant differences were detected in the two SNP sites between the male and female patients (P>0.05). Furthermore, no statistically significant differences were detected in rs2254137 genotype and allele distribution when comparing the male and female patients with their corresponding control groups (P>0.05). However, statistically significant differences were observed in the genotype and allele frequencies of rs16839883 when the male and female patients were compared with their respective controls (P<0.05). Therefore, the results demonstrated that there is a close correlation between the rs16839883 polymorphism in CREB1 and major depressive disorder, which suggests that this SNP site should be further studied as a potential biomarker for major depressive disorder.

Background: Evidence demonstrated diffusion-weighted imaging (DWI) lesions of different age predicted future stroke in transient ischemic attack (TIA) patients. The aim of this study is to develop a novel score (mABCD3-I) by replacing dual TIA with DWI lesions of different age and externally validate it in a multicenter TIA cohort. Methods: We conducted a prospective cohort study. The predictive outcome was stroke/all-cause death. Cox proportional hazards model was used to evaluate the predictive value of risk factors. The area under the curves (AUC) and net reclassification improvement (NRI) were used to present the discriminative and risk stratification abilities. Results: 2283 patients were included: 1077 in the derivation cohort and 1206 in the validation cohort. We derived mABCD3-I score by replacing dual TIA with DWI lesions of different age based on results of the multivariate analysis (Table 1). In the derivation cohort (Table 2), the AUCs for the mABCD3-I score were 0.78 at 90-day (95% confidence interval [CI]: 0.75-0.80; compared with ABCD3-I score, p=0.002), 0.78 at 6-month (95%CI: 0.75-0.81; p=0.008) and 0.78 at 1-year (95%CI: 0.75-0.81; p=0.018). The mABCD3-I score improved the reclassification at 90-day (p=0.006) and 6-month (p=0.033). In the validation cohort, the mABCD3-I had equal discriminative abilities compared with ABCD3-I score at 90-day (p=0.056) and 6-month (p=0.054), and higher ability at 1-year (p=0.044). Conclusions: Replacing dual TIA with DWI lesions of different age in ABCD3-I score improved risk prediction for stroke/death risk after TIA.