ABSTRACT
Objective:To explore the differences of the resting-state functional connectivity(FC) between goal-directed network and habituation networks in patients with early- and late-onset obsessive compulsive disorder (OCD) and the correlation between the strength of FC in the differential brain regions and cognitive flexibility.Methods:From October 2019 to April 2021, 40 patients with OCD were included in this study, including 22 patients with early-onset OCD and 18 patients with late-onset OCD.The cognitive flexibility of all subjects was assessed using the Wisconsin card sorting test (WCST), the Stroop task and the trail making test (TMT). The brain regions which were associated with goal-directed network(caudate, orbitofrontal cortex, ventromedial prefrontal cortex, and anterior cingulate cortex) and the brain regions which were associated with habituation network(putamen, supplementary motor area and insula) were selected as FC regions of interest (ROI). The DPABI and SPM12 plug-ins in the matlab2011a platform were used for whole brain FC analysis to compare the difference of FC between patients with early-onset OCD and patients with late-onset OCD on the two networks.The data were analyzed by SPSS 25.0 with χ2 test, independent samples t-test, and Pearson correlation analysis. Results:Compared with patients with early-onset OCD, patients with late-onset OCD had significantly enhanced FC of the left supplementary motor area with the left putamen and left insula.The total number of persistent errors of WCST in patients with late-onset OCD was greater than that in patients with early-onset OCD ((20.61±11.30), (14.95±8.94), P<0.05). The FC of the left putamen-left supplementary motor area was significantly and positively correlated with the total number of sustained responses ( r=0.678, P=0.003) and the total number of incorrect responses ( r=0.590, P=0.013) in patients with late-onset OCD.The FC of the left supplementary motor area-left insula was significantly positively correlated with the number of responses required to complete the first classification in patients with late-onset OCD ( r=0.485, P=0.049). Conclusion:Patients with late-onset OCD have stronger habituation network FC than patients with early-onset OCD, and the enhanced FC correlates with patients' cognitive flexibility performance, while late-onset OCD has more impaired cognitive flexibility than early-onset OCD.
ABSTRACT
Objective:The association between leptin receptor (LEPR) Q223R (Gln>Arg) gene polymorphism and systemic lupus erythematosus (SLE) remains controversial.In this study, a meta-analysis was used to comprehensively evaluate the association between LEPR Q223R gene polymorphism and SLE susceptibility.Methods:Case control studies on the relationship between LEPR Q223R gene polymorphism and SLE susceptibility were comprehensively searched by Medline (PubMed), Web of Science, CNKI, Wanfang digital journal full-text database, etc., and the search time was up to April 2020.The data of A/G allele frequency and AA/AG/GG genotype in SLE patients and healthy controls were extracted, the odds ratio ( OR) value and 95% confidence interval ( CI) were used as the combined effect-size indicators to analyze the correlation between allele, genotype and SLE risk.The heterogeneity among studies was analyzed quantitatively, and the publication bias was evaluated by Begg and Egger’s test. Results:A total of 7 case-control studies from 4 studies were retrieved.A total of 9 052 patients with SLE and 8 146 healthy controls were included in the meta-analysis.The results showed that there was no significant association between LEPR Q223R A/G gene polymorphism and SLE susceptibility, and the OR of A allele in LEPR Q223R gene locus associated with SLE risk was 1.03(95% CI: 0.92-1.14). The dominant (AA+ AG vs GG) and recessive (AA vs AG+ GG) models both suggested that LEPR Q223R A/G gene polymorphism was not associated with SLE, and the combined OR (95% CI) was 0.88(0.15-5.37) and 1.13(0.37-3.49), respectively.The results also showed that the distribution of LEPR Q223R genotype was different among different populations, and the inter-study heterogeneity was large. Conclusion:The existing evidence is insufficient to indicate that there is an association between LEPR Q223R A/G gene polymorphism and SLE susceptibility, which needs to be confirmed by further studies.
ABSTRACT
Objective To explore the role of aquaporin 1 (AQP1) in the initiation and development of hypertensive disorder complicating pregnancy ( HDCP), and to analyze the relationship between AQP1 expression and ascites formation of patients with eclampsia. Methods Sixty inpatients with HDCP were recruited in the study, including 20 patients with gestational hypertension, 20 with mild preeclampsia, and 20 with severe preeclampsia. And 20 healthy pregnant women were taken as control. Immunohistochemistry was used to analyze AQP1 expressions in placenta, embryolemma and peritoneum, and B-mode uhrasonography was used to detect the ascites level of the patients. Results ( 1 ) AQP1 expression was detected in placenta, embryolemma and peritoneum. AQP1 was mainly located in endotheliocytes of blood vessels and blood capillaries in placenta, endothelial cells of amniotic membrane in embryolemma, and endotheliocytes of blood capillary and small veins in peritoneum- (2)The ascites incidence of HDCP patients ( 63%, 38/60) was higher than that of controls( 10% ,2/20 ; P < 0. O1 ). ( 3 ) The positive expressive rate of AQP1 in placenta of patients with HDCP ( 85% ) was higher than that of controls ( 70%, P < 0. 01 ).Furthermore, the AQP1 positive expressive rate from severe preeclampsia (90%)was obviously higher than that from gestational hypertension patients ( 80%, P <0. 05 ). (4) The AQP1 positive expressive rate in embryolemma from HDCP patients( 87% ) was lower than that of controls ( 95%, P < 0. 05 ). The expressive rate from severe preeclampsia patients (80%) was obviously lower than that from gestational hypertension patients(95%, P <0. 05) and that of controls. (5) The AQP1 expressive rate in peritoneum from HDPC patients(82% )was higher than that of controls(70%, P <0. 01 ). The expressive rate of AQP1 from severe preeclampsia patients ( 90% ) was obviously higher than that from gestational hypertension patients (75%,P <0. 05) and that of controls. Conclusions The expression level of AQP1 of patients with preeclampsia increases in placenta and peritoneum and decreases in embryolemma, and holds correlation with the degree of HDCP. All these suggest that the changes in AQP1 expression may play an important role in the initiation and development of HDCP and may be one of the mechanisms for ascites formation.