Objective To investigate the relationship between 5 ,10-methylenetetrahydrofolate reductase (MTHFR) gene C677T locus polymorphism and unexplained adverse pregnancy.Methods Three hundreds and twenty pregnant women with unknown ad-verse pregnancy ≥ 2 times in the infertility department ,and obstetrics and gynecology department of our hospital from June 2014 to May 2016 were selected as the case group and 388 healthy non-abortion parous women were taken as the control group.The MTH-FR gene C677T locus polymorphism in the two groups was analyzed by using gene chip method.The differences in genotype and al-lele frequency distribution were compared between the two groups ,and the relationship between unexplained adverse pregnancy and MTHFR C677T locus polymorphism was analyzed.Results The frequency distribution of MTHFR genotype C677T C/C had sta-tistically significant difference between the case group and control group (P<0.05 ,OR=0.284).The frequency distribution of gen-otype C/T had no statistical difference between the case group and control group (P=0.400 ,OR=1.140).The frequency distribu-tion of genotype T/T had statistical difference between the case group and control group (P<0.05 ,OR=7.672).The frequency distribution of allele C and T had statistical difference between the case group and control group ( P< 0.05 ,OR= 0.304 ). Conclusion The high expression of MTHFR C677T genotype T/T may be a risk factor of unknown adverse pregnancy in child-bearing age women.

Objective:To describe demographic,clinical and physiological characteristics,treatment between first-episode major depressive disorder(MDD)and relapse MDD,and to explore characteristics of relapse MDD.Methods:Totally 858 patients who met the diagnostic criteria for depression of the Diagnostic and Statistical Manual of Mental Disorders,Fifth Edition(DSM-5),were included by using the Mini International Neuropsychiatric Interview(MINI),Clinician-Rated Dimensions of Psychosis Symptom Severity,and Hamilton Depression Scale etc.Among them,529(58.6％)were first-episode depression and 329(36.0％)were relapsed.The differences of demographic characteristics,clinical and physiological characteristics,treatment were compared byx2test and Kruskal-Wallis rank sum test.Multivariate logistic regression was used to explore the characteristics of MDD recur-rence.Results:Compared to first-episode MDD,relapse MDD had more comorbidity(OR=2.11,95％CI:1.00-4.44),more days out of role(OR=1.26,95％CI:1.01-1.56),more history of using psychiatric drug more than one month(OR=1.41,95％CI:1.02-1.97)and electroconvulsive therapy(OR=3.23,95％CI:1.42-7.36),and higher waist-hip ratio(OR=33.88,95％CI:2.88-399.32).Conclusion:Relapse MDD has positive as-sociation with comorbidity of mental disorders,out of role,and higher waist-hip ratio.

Detailed characterizations of genomic alterations have not identified subtype-specific vulnerabilities in adult gliomas. Mapping gliomas into developmental programs may uncover new vulnerabilities that are not strictly related to genomic alterations. After identifying conserved gene modules co-expressed with EGFR or PDGFRA (EM or PM), we recently proposed an EM/PM classification scheme for adult gliomas in a histological subtype- and grade-independent manner. By using cohorts of bulk samples, paired primary and recurrent samples, multi-region samples from the same glioma, single-cell RNA-seq samples, and clinical samples, we here demonstrate the temporal and spatial stability of the EM and PM subtypes. The EM and PM subtypes, which progress in a subtype-specific mode, are robustly maintained in paired longitudinal samples. Elevated activities of cell proliferation, genomic instability and microenvironment, rather than subtype switching, mark recurrent gliomas. Within individual gliomas, the EM/PM subtype was preserved across regions and single cells. Malignant cells in the EM and PM gliomas were correlated to neural stem cell and oligodendrocyte progenitor cell compartment, respectively. Thus, while genetic makeup may change during progression and/or within different tumor areas, adult gliomas evolve within a neurodevelopmental framework of the EM and PM molecular subtypes. The dysregulated developmental pathways embedded in these molecular subtypes may contain subtype-specific vulnerabilities.
Humans ; Brain Neoplasms/pathology* ; Neoplasm Recurrence, Local/metabolism* ; Glioma/pathology* ; Neural Stem Cells/pathology* ; Oligodendrocyte Precursor Cells/pathology* ; Tumor Microenvironment