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BACKGROUND The striatum has been reported to be implicated in various neurological diseases, including lifelong premature ejaculation (LPE). Altered striatum-related functional connectivity was investigated in LPE patients in previous studies; however, structural abnormalities in the striatum have been less studied in LPE. PURPOSE To identify the gray matter volume (GMV) and structural covariance patterns of the striatum between LPE patients and healthy controls (HCs). STUDY TYPE Prospective. SUBJECTS Forty-three LPE patients and 31 male HCs. FIELD STRENGTH/SEQUENCE 3.0 T magnetic resonance imaging (MRI) scanner; T1-weighted imaging using a spoiled gradient recalled echo sequence. ASSESSMENT Preprocessing of structural MRI data and the striatum-seeded GMV computation were conducted using SPM12. STATISTICAL TESTS Two sample t-test was used to compare differences in GMV of the striatum between patients and HCs. Regions showing altered between-group GMV were considered as seeds for structural covariance analysis in two groups. Additionally, correlations between GMV findings and clinical features were assessed with age and total intracranial volume (TIV) as covariates and with age, TIV, anxiety, and depression scores as covariates in the patient group, P

To investigate abnormal intrinsic connectivity of striatum in lifelong premature ejaculation (PE) patients compared with healthy controls (HCs).Forty-seven lifelong PE patients and 30 healthy controls were enrolled in the present study and underwent resting-state functional magnetic resonance imaging. The functional connectivity (FC) analysis and 2-sample t tests were applied to investigate the alterations of striatum-related connectivity in patients compared with HCs (significant threshold at P.05, false discovery rate corrected), and during which Fisher's r-to-z transformation was adopted and the resulting z values were used as the statistical FC values. Correlation analysis was performed to test possible relationships between the imaging findings and clinical characteristics in the patient group (P.05, Bonferroni correction).The results showed that compared with HCs, lifelong PE patients had significantly decreased FC between the right caudate and insula, superior temporal pole (STP) and orbitofrontal cortex (OFC) as well as decreased FC between the bilateral putamen and insula, STP and middle cingulate cortex (MCC). Meanwhile, patients had significantly increased FC between the left caudate and OFC, and increased FC between the right putamen and fusiform. The mean FC value from the caudate-OFC, caudate-insula, and caudate-STP connectivity negatively correlated with the Premature Ejaculation Diagnostic Tool score, separately.The current study showed the functional abnormality of lifelong PE in multiple brain regions implicated in sensation, motivation, and ejaculation-related inhibitory control, which may improve our understanding of the abnormal striatum-related neural mechanisms in lifelong PE patients.

Background. Pulmonary ischemia reperfusion- (I/R-) induced dysfunction is a significant clinical problem after lung transplantation. In this study, we aim to explore the molecular mechanism of lung I/R injury (LIRI). Methods. Bioinformatic analysis of gene involved in oxidative stress. A HUVEC oxygen glucose deprivation/reoxygenation (OGD/R) model and I/R mouse model were first established via I/R. The cellular proliferation, migration, reactive oxygen species (ROS), and parameters of lung injury were assessed via CCK-8, EdU staining, Transwell, cellular ROS kit, and H&E staining. We also confirmed related gene expressions and protein levels and the interaction between the tissue factor pathway inhibitor (TFPI) promotor and ZNF354C. Results. Bioinformatic analysis results showed TFPI contributed to oxidative stress. OGD/R caused a reduction in cell viability and migration, hypermethylation of TFPI, increased ROS, and downregulation of ZNF354C, TFPI, and DNA methyltransferases (DNMTs) in HUVECs. Besides, ZNF354C could directly bind to the TFPI promoter, enhance proliferation and migration, and inhibit ROS in OGD/R-induced HUVECs by upregulating TFPI. More importantly, we discovered that 5-Aza could reduce TFPI methylation, upregulate TFPI, and enhance the binding of ZNF354C to the TFPI promoter in LIRI. Furthermore, DNMT1 silencing could induce proliferation and migration and prevent ROS in OGD/R-induced HUVECs by upregulating ZNF354C. Additionally, we verified that ZNF354C could alleviate LIRI by preventing DNA methylation in vivo. Conclusions. ZNF354C overexpression induced proliferation and migration, as well as suppressed ROS in OGD/R-induced HUVECs, and alleviated LIRI in mice by inhibiting TFPI promoter methylation to upregulate TFPI. Therefore, ZNF354C and TFPI methylation might be promising molecular markers for LIRI therapy.

Lifelong premature ejaculation (PE) is one of the most prevalent male sexual dysfunctions. It is still not well known about the possible neural mechanisms of lifelong PE. This study tried to investigate the abnormal characteristics of brain functional networks of lifelong PE and to assess relationships of PE-related functional abnormalities with clinical symptoms. Functional magnetic resonance imaging (fMRI) data and clinical symptoms were collected from 45 lifelong PE patients and 37 healthy controls (HCs) since 2016, including disease and sexual life history, intravaginal ejaculatory latency time measured by stopwatch and other scales. The degree centrality (DC) approach were applied to distinguish altered brain functions between the two groups (p 0.05, false discovery rate corrected). Correlation analysis was then performed to examine relationships between the imaging findings and clinical symptoms (p 0.05, Bonferroni corrected). Results showed that compared with HCs, lifelong PE patients had increased DC value in the medial prefrontal cortex (mPFC), precuneus and primary somatosensory cortex (SI) as well as decreased DC value in the insula and orbitofrontal cortex. After controlling for anxiety and depression levels, the significant difference in the mPFC was not found. The DC value in the SI positively correlated with premature ejaculation diagnostic tool (PEDT) score in the patients. The present findings indicate that lifelong PE patients have altered DC in brain regions involved in sensation, motivation and inhibitory control processing. Our study may improve our understanding and provide a new sight into the further research of lifelong PE.

BACKGROUND The aim of this study was to further clarify the effects of valsartan on restenosis in patients with arteriosclerosis obliterans of the lower extremities. MATERIAL AND METHODS Patients with arteriosclerosis obliterans of the lower extremities undergoing continuous stent implantation in the superficial femoral artery were enrolled and randomly divided into an ARB group and a control group. Patients in the ARB group received valsartan orally in a single-blind manner and were followed up for 6 months. An evaluation was performed based on the criteria for clinical efficacies designed by the Committee of Vascular Disease, Chinese Association of Integrative Medicine. The total clinical effective rate was calculated, and ankle brachial index (ABI) of the patients was assessed. The concentrations of interleukin-6 (IL-6) and high-sensitivity C-reactive protein (hs-CRP) were measured using enzyme-linked immunosorbent assay. The in-stent restenosis of patients was examined by angiography. RESULTS One patient in the control group died due to acute cerebral hemorrhage 4 months after enrollment, and 1 patient was lost to follow-up due to acute myocardial infarction during follow-up 5 months after enrollment. Age, sex, Fontaine stage, and underlying diseases were comparable between the 2 groups. Hs-CRP (3.93±1.43) and IL-6 (11.26±2.29) levels were significant different in the ARB group compared with the control group. The postoperative follow-up showed that ABI was 0.98±0.20 in the ARB group and 0.62±0.48 in the control group. CONCLUSIONS Valsartan inhibited the increase in hs-CRP and IL-6 levels, improved clinical efficacies, increased ABI, and decreased the restenosis rate after the interventional therapy in patients with arteriosclerosis obliterans of the lower extremities.

BACKGROUND As one of the most prevalent sexual dysfunctions in men, lifelong premature ejaculation (PE) often leads to patient distress. The hypothalamus is implicated in the ejaculatory control of healthy males. However, we do not know whether the hypothalamus-related intrinsic connectivity is altered in lifelong PE patients. PURPOSE To investigate abnormal intrinsic connectivity of the hypothalamus in lifelong PE patients compared with healthy controls (HCs). STUDY TYPE Prospective pilot study using cross-sectional data of patients and HCs. SUBJECTS Forty-seven lifelong PE patients and 30 HCs were included in this study. FIELD STRENGTH/SEQUENCE 3.0T MRI scanner for T1 -weighted imaging using spoiled gradient recalled echo sequence and functional imaging using a single-shot gradient recalled echo sequence. ASSESSMENT Preprocessing of MRI data and hypothalamus-seeded functional connectivity (FC) computation were performed using DPABI4.1. STATISTICAL TESTS The two-sample t-test within SPM12 was adopted to examine possible alterations of intrinsic connectivity of hypothalamus in lifelong PE patients compared with HCs including anxiety and depression scores as covariates (false discovery rate-corrected, P

Premenstrual syndrome (PMS) is a menstrual cycle-related disorder. Although the precise pathophysiology is not fully understood, it is increasingly believed that the central nervous system plays a vital role in the development of PMS. The aim of this study is to elucidate specific functional connectivity between the thalamus and cerebral cortex. Resting-state functional magnetic resonance imaging (fMRI) data were obtained from 20 PMS patients and 21 healthy controls (HCs). Seed-based functional connectivity between the thalamus and six cortical regions of interest, including the prefrontal cortex (PFC), posterior parietal cortex, somatosensory cortex, motor cortex/supplementary motor area, temporal and occipital lobe, was adopted to identify specific thalamocortical connectivity in the two groups. Correlation analysis was then used to examine relationships between the neuroimaging findings and clinical symptoms. Activity in distinct cortical regions correlated with specific sub-regions of the thalamus in the two groups. Comparison between groups exhibited decreased prefrontal-thalamic connectivity and increased posterior parietal-thalamic connectivity in the PMS patients. Within the PMS group, the daily record of severity of problems (DRSP) score negatively correlated with the prefrontal-thalamic connectivity. Our findings may provide preliminary evidence for abnormal thalamocortical connectivity in PMS patients and may contribute to a better understanding of the pathophysiology of PMS.

Background Denatonium, a widely used bitter agonist, activates bitter taste receptors on many cell types and plays important roles in chemical release, ciliary beating and smooth muscle relaxation through intracellular Ca2+-dependent pathways. However, the effects of denatonium on the proliferation of airway epithelial cells and on the integrity of cellular components such as mitochondria have not been studied. In this study, we hypothesize that denatonium might induce airway epithelial cell injury by damaging mitochondria. Methods Bright-field microscopy, cell counting kit-8 (CCK-8) assay and flow cytometry analysis were used to examine cellular morphology, proliferation and cell cycle, respectively. Transmission electron microscopy (TEM) was used to examine mitochondrial integrity. JC-1 dye and western blotting techniques were used to measure mitochondrial membrane potential and protein expression, respectively. Results For airway epithelial cells, we observed that denatonium significantly effects cellular morphology, decreases cell proliferation and reduces the number of cells in S phase in a dose-dependent manner. TEM analysis demonstrated that denatonium causes large amplitude swelling of mitochondria, which was confirmed by the loss of mitochondrial membrane potential, the down-regulation of Bcl-2 protein and the subsequent enhancement of the mitochondrial release of cytochrome c and Smac/DIABLO after denatonium treatment. Conclusions In this study, we demonstrated for the first time that denatonium damages mitochondria and thus induces apoptosis in airway epithelial cells. Electronic supplementary material The online version of this article (doi:10.1186/s12931-015-0183-9) contains supplementary material, which is available to authorized users.