18 research outputs found

    Brain structural network topological alterations of the left prefrontal and limbic cortex in psychogenic erectile dysfunction

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    <p><b>Aim:</b> Despite increasing understanding of the cerebral functional changes and structural abnormalities in erectile dysfunction, alterations in the topological organization of brain networks underlying psychogenic erectile dysfunction remain unclear.</p> <p><b>Materials and methods:</b> Here, based on the diffusion tensor image data of 25 patients and 26 healthy controls, we investigated the topological organization of brain structural networks and its correlations with the clinical variables using the graph theoretical analysis.</p> <p><b>Results:</b> Patients displayed a preserved overall small-world organization and exhibited a less connectivity strength in the left inferior frontal gyrus, amygdale and the right inferior temporal gyrus. Moreover, an abnormal hub pattern was observed in patients, which might disturb the information interactions of the remaining brain network. Additionally, the clustering coefficient of the left hippocampus was positively correlated with the duration of patients and the normalized betweenness centrality of the right anterior cingulate gyrus and the left calcarine fissure were negatively correlated with the sum scores of the 17-item Hamilton Depression Rating Scale.</p> <p><b>Conclusions:</b> These findings suggested that the damaged white matter and the abnormal hub distribution of the left prefrontal and limbic cortex might contribute to the pathogenesis of psychogenic erectile dysfunction and provided new insights into the understanding of the pathophysiological mechanisms of psychogenic erectile dysfunction.</p

    Data_Sheet_1_Impaired Prefrontal-Amygdala Pathway, Self-Reported Emotion, and Erection in Psychogenic Erectile Dysfunction Patients With Normal Nocturnal Erection.docx

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    <p>Background: Neuroimaging studies have demonstrated that the prefrontal cortex and amygdala play an important role in sexual arousal (SA). However, little is known about the interactions between the prefrontal and cortex amygdala, which mediate the cognitive regulation of emotion and SA.</p><p>Objective: We seek to determine whether nocturnal erection of psychogenic erectile dysfunction (pED) patients are normal and whether there are changes of topological organization in the prefrontal-amygdala pathway of brain network in pED. In addition, whether there are correlations between network property changes and self-reported emotion and erection.</p><p>Design, setting, and participants: We used the RigiScan device to evaluate erectile function of patients and employed diffusion MRI and graph theory to construct brain networks of 21 pED patients and 24 healthy controls.</p><p>Outcome measurements and statistical analysis: We considered four nodal metrics and their asymmetry scores, and nocturnal penile tumescence (NPT) parameters, to evaluate the topological properties of brain networks of pED and their relationships with the impaired self-reported emotion and erection.</p><p>Results and limitations: All the pED patients showed normal nocturnal penile erection, however impaired self-reported erection and negative emotion. In addition, patients showed lower connectivity degree and strength in the left prefrontal-amygdala pathway. We also found that pED exhibited lower leftward asymmetry in the inferior frontal gyrus. Furthermore, patients showed more hub regions and fewer pivotal connections. Moreover, the degree of the left amygdala of pED showed significantly negative correlation with the self-reported erection and positive correlation with the self-reported negative emotion.</p><p>Conclusions: Together, these results suggest normal nocturnal erection in pED. However, abnormalities of brain network organization in pED, particularly in the left prefrontal-amygdala pathway, are associated with the impaired self-reported erection and negative emotion.</p

    Urodynamic experimental parameters of rats in each group ( ± S).

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    <p>DM group and Control group: p<0.01; DM group and DM/TENS group p<0.05; p<0.01.</p><p>DM group and DM/TENS group: p<0.05; p<0.01. DM/TENSDM/TENS group and Control group: p<0.05; p<0.01.</p

    Tube formation of human umbilical vein endothelial cells (HUVECs) treated by the conditioned medium derived from ADEPCs, ADSCs and RBSMCs.

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    <p><b>(A)</b> Representative photomicrographs of tube formation of HUVECs treated by different medium. Scale bar = 100 μm. (B) Quantitative analyses of tube formation of HUVECs among different treatments. The results were expressed as fold change of the control (*p<0.05, #p>0.05, n = 6).</p

    General information of the rats (± S).

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    <p>In 10<sup>th</sup> and 13<sup>th</sup> week: contrast group to group, blood sugar is obviously increased and body weight is obviously decreased (p<0.01).contrast group and, body weight and blood sugar are not statistically different (p>0.05). Contrast group to group, the bladder wet weight is obviously increased, and after the treatment, the bladder wet weight of group is obviously increased (p<0.01).</p

    mRNA content of CGRP in rats DRG of each group.

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    <p><sup>*)</sup>DM/TENS group and DM group P<0.01.</p><p><sup>**)</sup>DM/TENS group and Control group P<0.05.</p

    Growth characteristics of ADEPCs, ADSCs and RBSMCs.

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    <p><b>(A)</b> Cell proliferation curve showed that all the three kinds of cells had similar growth pattern. <b>(B)</b> The PD at passage 1 and 5 of ADEPCs (10.1±1.2 and 10.9±1.5) were significantly higher than that of ADSCs (6.3±0.7 and 6.9±1.1) and RBSMCs (4.9±0.8 and 5.1±0.9) (*p<0.05, n = 6). <b>(C)</b> The DT at passage 1 and 5 of ADEPCs (35.7±4.6 hours and 33.8±4.2 hours) were significantly lower than that of ADSCs (52.6±6.3 hours and 51.7±5.9 hours) and RBSMCs (64.8±8.2 hours and 64.2±7.1 hours) (*p<0.05, n = 6).</p

    Quantification of cAMP concentration of the bladder in rats DRG of each group (**<i>P</i><0.01 VS DM/TENS group, *<i>P</i><0.05 VS DM/TENS group).

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    <p>Quantification of cAMP concentration of the bladder in rats DRG of each group (**<i>P</i><0.01 VS DM/TENS group, *<i>P</i><0.05 VS DM/TENS group).</p

    Quantification of CGRP protein level in rats bladder wall (A&C)and DRG(B&D) in control, DM and DM/TENS group, (**<i>P</i><0.01 VS DM/TENS group, *<i>P</i><0.05 VS DM/TENS group).

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    <p>Quantification of CGRP protein level in rats bladder wall (A&C)and DRG(B&D) in control, DM and DM/TENS group, (**<i>P</i><0.01 VS DM/TENS group, *<i>P</i><0.05 VS DM/TENS group).</p

    Tube formation apability of ADEPCs at passage 1 and 5.

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    <p><b>(A)</b> Representative photomicrographs of tube formation of ADEPCs at passage 1 (P1) and 5 (P5). Scale bar = 100 μm. <b>(B)</b> There was no significant difference on the capability of tube formation of ADEPCs between passage 1 and 5 (p>0.05, n = 6).</p
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