Altered voxel-level whole-brain functional connectivity in multiple system atrophy patients with depression symptoms.

BACKGROUND: It is yet unknown if the whole-brain resting-state network is altered in multiple system atrophy with symptoms of depression. This study aimed to investigate if and how depression symptoms in multiple system atrophy are associated with resting-state network dysfunction. METHODS: We assessed the resting-state functional network matric using Degree centrality (DC) coupling with a second ROI-wise functional connectivity (FC) algorithm in a multimodal imaging case-control study that enrolled 32 multiple system atrophy patients with depression symptoms (MSA-D), 30 multiple system atrophy patients without depression symptoms (MSA-ND), and 34 healthy controls (HC). RESULTS: Compared to HC, MSA-D showed more extensive DC hub dysfunction in the left precentral and right middle frontal cortex than MSA-ND. A direct comparison between MSA-D and MSA-ND detected increased DC in the right anterior cingulum cortex, but decreased DC in the left cerebellum lobule IV and lobule V, left middle pole temporal cortex, and right superior frontal cortex. Only right anterior cingulum cortex mean DC values showed a positive correlation with depression severity, and used ACC as seed, a second ROI-wise functional connectivity further revealed MSA-D patients showed decreased connectivity between the ACC and right thalamus and right middle temporal gyrus (MTG). CONCLUSIONS: These findings revealed that dysfunction of rACC, right middle temporal lobe and right thalamus involved in depressed MSA. Our study might help to the understanding of the neuropathological mechanism of depression in MSA.

Quantitative assessment of maternal common carotid artery mechanics using velocity vector imaging in pre-eclampsia.

OBJECTIVE: Velocity vector imaging (VVI) is widely used to quantify cardiac mechanical deformation. This study sought to determine whether VVI could be used to evaluate the stiffness of maternal peripheral arteries in women with pre-eclampsia. STUDY DESIGN: Twenty-four women with pre-eclampsia and 34 normotensive pregnant women were recruited. Longitudinal and circumferential peak velocity, strain and strain rate of the right common carotid artery (CCA) were measured. All measurements were averaged from three consecutive cardiac cycles and expressed as mean ± standard deviation. RESULTS: Longitudinal velocity, strain and strain rate of the anterior and posterior walls of the CCA were significantly lower in women with pregnancy-induced hypertension compared with normotensive pregnant women [velocity: 0.22 ± 0.09 cm/s vs 0.29 ± 0.09 cm/s (p<0.01) and 0.24 ± 0.10 cm/s vs 0.34 ± 0.13 cm/s (p<0.01); strain: 8.50 ± 4.92% vs 12.2 ± 6.21% (p<0.01) and 10.11 ± 5.02% vs 14.21 ± 6.48% (p<0.05); strain rate: 1.62 ± 1.14 s(-1) vs 2.24 ± 1.13 s(-1) (p<0.05) and 1.91 ± 0.99 s(-1) vs 2.45 ± 0.97 s(-1) (p<0.05)]. Similar results were also found for circumferential velocity, strain and strain rate of the anterior and posterior walls, and the interior and exterior lateral walls of the CCA. CONCLUSIONS: Stiffness of the maternal CCA was significantly greater in women with pre-eclampsia compared with normotensive pregnant women. VVI may have potential for quantitative assessment of vascular mechanical deformation in the clinical setting.

Overexpression of miR-152 leads to reduced expression of human leukocyte antigen-G and increased natural killer cell mediated cytolysis in JEG-3 cells.

OBJECTIVE: The purpose of this study was to gain a further understanding of the relationship between miR-152 and human leukocyte antigen (HLA)-G in human trophoblast cell line (JEG-3). STUDY DESIGN: The JEG-3 cells were transfected with pre-miR-152. The effect of the overexpressed miR-152 on HLA-G expression, trophoblast invasion, and natural killer (NK) cell-mediated cytolysis were assessed by reverse-transcription polymerase chain reaction (RT-PCR) and Western blot analysis, transwell invasion assay, and NK cell cytotoxicity assay, respectively. RESULTS: The miR-152 repressed HLA-G expression but exerted no effect on JEG-3 cell invasion, and overexpression of miR-152 led to increased NK cell-mediated cytolysis in JEG-3 cells. CONCLUSION: The data indicate that miR-152 may function as an immune system enhancer through up-regulating NK cell-mediated cytolysis of host cells.