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The aim of the study was to compare the magnetic resonance imaging (MRI) findings of intracranial haemorrhage (ICH) in the middle- and late trimesters and to explore the relationship between the MRI features of foetal ICH and postnatal outcomes. This was a retrospective study which recruited foetal ICH diagnosed by MRI in one tertiary centre from 2015 to 2019. The prenatal and postnatal medical records were reviewed. Of 39 ICH cases, 82.1% (32) had germinal matrix intraventricular haemorrhage (GM-IVH), and 18.9% (7) were diagnosed with non-GM-IVH. The cerebellum, corpus callosum and subdural space were affected in 5, 1 and 1 non-GM-IVH cases, respectively. MRI confirmed possible ICH on sonogram in 10 cases (35.7%) and the remaining 19 added ICH diagnoses that were not obtained on initial ultrasound imaging. Pregnancy outcome data were available in 82.1% of (32) cases, of which 21 were terminated pregnancies, 1 was foetal demise and 10 were delivered. One neonate died after birth and one infant suffered from hearing loss. The remaining eight patients had favourable outcome. In our study, evaluation of the relationship between MRI findings and outcomes remains challenging, depending on the timing of examination and the hematoma itself. MRI was an adjunct to US in diagnosing ICH in utero which helps to assess postnatal development.

Background Idiopathic hypogonadotropic hypogonadism (IHH) is a rare genetic disease attributed to the disorder of hypothalamic-pituitary-gonadal axis. Mutations in the GNRHR gene are one of the most common genetic causes of IHH. Herein, we aimed to investigate GNRHR variants in a Chinese cohort with IHH, and to characterize them at the molecular level. Methods A total of 153 IHH patients were recruited, and variants were detected using a tailored next-generation sequencing panel. GNRHR rare sequencing variant (RSV) was verified using Sanger sequencing. Phenotypic features and therapeutic outcomes of patients were followed up. In order to examine the pathogenicity of the GNRHR RSV, we performed conservative analysis, crystal structure prediction, expression analysis as well as the assessment of ERK1/2 activation and IP3/Ca2+ response. Results The same heterozygous RSV (p.R240Q) in GNRHR was identified in four sporadic IHH patients. These patients exhibited different severity of testicular development and hormone profile. hCG treatment was effective in improving gonadal development, serum testosterone, and semen quality. The GNRHR RSV has no effect on the expression of mRNA and protein, whereas damaged ERK1/2 activation and inositol triphosphate/calcium signaling. Conclusions The study expands GNRHR mutation spectrum in IHH patients, and reveals that the GNRHR RSV is a partial loss-of-function mutation. Although this heterozygous RSV may not have a significant influence on the pathogenesis of IHH, but its homozygous/ compound status should be paid attention in this research field.

To estimate human fetal brain MRI tissue properties including apparent T1 (T1app) and apparent proton density (PDapp) by using a rapid multi-contrast acquisition protocol called STrategically Acquired Gradient Echo (STAGE) imaging. STAGE data were collected using two flip angles (15° and 60°, with a TR = 600 ms) for 30 pregnant women at 1.5 T (15 healthy controls: gestational age (GA) range 19 + 1/7 weeks to 34 + 5/7 weeks; 11 abnormal subjects with ventriculomegaly: GA range 21 + 5/7 weeks to 31 + 5/7 weeks; 4 subjects with other abnormalities). Both T1app and PDapp maps of the fetal brain were calculated from the STAGE data. A region-of-interest-based approach was used to measure T1app and PDapp in the subplate/intermediate zone (SP/IZ), cortical plate (CP), and cerebrospinal fluid (CSF) in the fetal brain. The ratios of T1appSP/IZ/T1appCP and PDappSP/IZ/PDappCP were larger than unity while T1appSP/IZ/T1appCSF and PDappSP/IZ/PDappCSF were both less than unity. STAGE imaging provides a potential practical approach to estimate multi-parametric properties of the human fetal brain. • STAGE is feasible in measuring fetal brain tissue properties. • Water content in cortical plate and subplate/intermediate zone approaches that of cerebrospinal fluid in early gestational ages.

Prostate cancer is one of the deadliest cancers in men. RNA-binding proteins play a critical role in human cancers; however, whether they have a significant effect on the prognosis of prostate cancer has yet to be elucidated. In the present study, we performed a comprehensive analysis of RNA sequencing and clinical data from the Cancer Genome Atlas dataset and obtained differentially expressed RNA-binding proteins between prostate cancer and benign tissues. We constructed a protein-protein interaction network and Cox regression analyses were conducted to identify prognostic hub RNA-binding proteins. SNRPA1 was associated with the highest risk of poor prognosis and was therefore selected for further analysis. SNRPA1 expression was positively correlated with Gleason score and pathological TNM stage in prostate cancer patients. Furthermore, the expression profile of SNRPA1 was validated using the Oncomine, Human Protein Atlas, and Cancer Cell Line Encyclopedia databases. Meanwhile, the prognostic profile of SNRPA1 was successfully verified in GSE70769. Additionally, the results of molecular experiments revealed the proliferative role of SNRPA1 in prostate cancer cells. In summary, our findings evidenced a relationship between RNA-binding proteins and prostate cancer and indicated the prognostic significance of SNRPA1 in prostate cancer.

Prostate cancer (PCa) is one of the most deadly urinary tumors in men globally, and the 5‐year over survival is poor due to metastasis of tumor. It is significant to explore potential biomarkers for early diagnosis and personalized therapy of PCa. In the present study, we performed an integrated analysis based on multiple microarrays in the Gene Expression Omnibus (GEO) dataset and obtained differentially expressed genes (DEGs) between 510 PCa and 259 benign issues. The weighted correlation network analysis indicated that prognostic profile was the most relevant to DEGs. Then, univariate and multivariate COX regression analyses were conducted and four prognostic genes were obtained to establish a four‐gene prognostic model. And the predictive effect and expression profiles of the four genes were well validated in another GEO dataset, The Cancer Genome Atlas and the Human Protein Atlas datasets. Furthermore, combination of four‐gene model and clinical features was analyzed systematically to guide the prognosis of patients with PCa to a largest extent. In summary, our findings indicate that four genes had important prognostic significance in PCa and combination of four‐gene model and clinical features could achieve a better prediction to guide the prognosis of patients with PCa., Prostate cancer (PCa) is one of the most deadly urinary tumors in men globally, and the progression and development of PCa is associated with copious genetic aberrations. This study is aimed to add novel biomarkers of PCa development and prognosis by analyzing the genetic changes and clinical traits comprehensively. Based on integrated analysis, four genes were significantly related to the prognosis of PCa and well validated in other datasets. Furthermore, combination of four genes and clinical features achieved a better prediction to guide the prognosis of patients with PCa.

Erectile dysfunction (ED) is a major health issue among men with diabetes, and ED induced by diabetes mellitus (DMED) is particularly difficult to treat. Therefore, novel therapeutic approaches for the treatment of DMED are urgently needed. Exosomes, nanosized particles involved in many physiological and pathological processes, may become a promising tool for DMED treatment. In this study, we investigated the therapeutic effect of exosomes derived from corpus cavernosum smooth muscle cells (CCSMC‐EXOs) on erectile function in a rat model of diabetes and compared their effect with that of exosomes derived from mesenchymal stem cells (MSC‐EXOs). We incubated labelled CCSMC‐EXOs and MSC‐EXOs with CCSMCs and then observed uptake of the exosomes at different time points using laser confocal microscopy. CCSMC‐EXOs were more easily taken up by CCSMCs. The peak concentration and retention time of labelled CCSMC‐EXOs and MSC‐EXOs in the corpus cavernosum of DMED rats after intracavernous injection were compared by in vivo imaging techniques. Intracavernous injection of CCSMC‐EXOs was associated with a relatively high peak concentration and long retention time. Our data showed that CCSMC‐EXOs could improve erectile function in DMED rats. Meanwhile, CCSMC‐EXOs could exert antifibrotic effects by increasing the smooth muscle content and reducing collagen deposition. CCSMC‐EXOs also increased the expression of eNOS and nNOS, followed by increased levels of NO and cGMP. These findings initially identify the possible role of CCSMC‐EXOs in ameliorating DMED through inhibiting corporal fibrosis and modulating the NO/cGMP signalling pathway, providing a theoretical basis for a breakthrough in the treatment of DMED.

BACKGROUND The population with diabetes mellitus-induced erectile dysfunction is increasing rapidly, but current drugs are not effective in treating erectile dysfunction. Studies of the traditional Chinese medicine extract berberine on diabetes and its complications provide us with new ideas. OBJECTIVES To evaluate the therapeutic effect and potential mechanism of berberine on the erectile function of diabetic rats. MATERIALS AND METHODS Fifty male Sprague-Dawley rats were randomly grouped, and 42 rats were injected intraperitoneally with streptozotocin to establish a diabetes model. Erectile dysfunction rats were screened out through the apomorphine test and randomly divided into the diabetes mellitus and berberine groups, and these animals were administered berberine (200 mg/kg/day) and normal saline by gavage for 4 weeks. Primary corpus cavernous smooth muscle cells from healthy rats were cultured and treated with berberine. RESULTS Fasting blood glucose in the diabetes mellitus group was significantly increased, while berberine showed no significant effect on glucose. Erectile function was obviously impaired in the diabetes mellitus group, and berberine administration partially rescued this impairment. The expression of sphingosine kinase 1, S1PR2, and sphingosine-1-phosphate in the diabetes mellitus group was increased. Berberine partially inhibited the expression of sphingosine kinase 1 and S1PR2, but the decrease in sphingosine-1-phosphate was not significant. Moreover, mitogen-activated protein kinase pathway factor expression was upregulated and eNOS activity was decreased in the diabetes mellitus group. Berberine treatment could partially reverse these alterations. Severe fibrosis and apoptosis were detected in diabetic rats, accompanied by higher expression of TGFβ1, collagen I/IV, Bax/Bcl-2, and caspase 3 than in the other groups. However, supplementation with berberine inhibited the expression of these proteins and attenuated fibrosis and apoptosis. CONCLUSIONS Berberine ameliorated erectile dysfunction in rats with diabetes mellitus, possibly by improving endothelial function and inhibiting apoptosis and fibrosis by suppressing the sphingosine kinase 1/sphingosine-1-phosphate/S1PR2 and mitogen-activated protein kinase pathways.

Background Oxidative stress is a significant contributor to the poor treatment efficacy on erectile dysfunction induced by diabetes mellitus (DMED). Thus, understanding the mechanism underlying oxidative stress will aid in the identification of novel therapeutic targets. Aim To define the role of Janus kinase 2 (JAK2) in mediating oxidative stress in the corpus cavernosum smooth muscle cells (CCSMCs) and to investigate the therapeutic effect of monomeric berberine (BB), which inhibits JAK2, in the pathogenesis of DMED. Methods Streptozotocin was used to establish type I diabetic rat models and apomorphine tests were conducted to determine DMED rats. Eighteen DMED rats were divided into the DMED group and the DMED+BB group, whereas another 10 age-matched rats formed the control group. CCSMCs were isolated from the corpus cavernosum of rats and were treated with the JAK2 inhibitor alpha cyanano-(3,4-hydroxyl)N-benzophenylamine (AG490) and/or BB. Outcomes Metabolic parameters; erectile function; histologic and molecular alterations. Results Erectile function was impaired and excessive oxidative stress was found in the DMED group. Excessive oxidative stress led to decreased expression level of phosphorylated endothelial nitric oxide synthase at serine 1177/endothelial nitric oxide synthase and increased expression level of Ras homolog gene family and Rho kinase 1/2. Meanwhile, the relative expression ratio of phosphorylated JAK2/JAK2 was significantly greater in the DMED group than that in the other groups. In vitro, oxidative stress was significantly reduced along with reduced intracellular calcium upon treatment with the JAK2 inhibitor, AG490. Moreover, the CCSMCs treated with BB showed changes similar to those upon treatment with AG490. In vivo experiments also confirmed that the erectile function of the DMED+BB group was improved, accompanied by decreased phosphorylated JAK2/JAK2 and decreased oxidative stress. Clinical Translation JAK2 can be used as a therapeutic target and BB can be used as a potential drug for the clinical treatment of DMED. Strengths and Limitations This study examines the promoting effect of JAK2 on oxidative stress occurrence in the corpus cavernosum and on the development of DMED in both animal experiments and cell experiments, as well evaluates the inhibitory effect of BB on JAK2 and its therapeutic effect on DMED. The main limitation of our current study is the lack of an appropriate means for activating JAK2. Conclusions JAK2 can induce DMED by enhancing oxidative stress and BB can play a role in treating DMED by inhibiting JAK2 and reducing oxidative stress. Our study provides an option and an idea for further studies on the pathogenesis and treatment of DMED.

Background To determine whether magnetic resonance (MR) imaging features combined with apparent diffusion coefficient (ADC) values could be used as a tool for categorizing ovarian epithelial cancer (OEC) and predicting survival, as well as correlating with laboratory tests (serum cancer antigen 125, serum CA-125) and tumor proliferative index (Ki-67 expression). Methods and materials MRI examination was undertaken before invasive procedures. MRI features were interpreted and recorded on the picture archive communication system (PACS). ADC measurements were manually performed on post-process workstation. Clinical characteristics were individually retrieved and recorded through the hospital information system (HIS). Cox hazard model was used to estimate the effects of both clinical and MRI features on overall survival. Results Both clinical and MRI features differed significantly between Type I and Type II cancer groups (p

Rationale and objectives The goal of this study was to estimate venous blood oxygen saturation (SvO2) in the superior sagittal sinus (SSS) in fetal brains with ventriculomegaly (VM) using quantitative susceptibility mapping (QSM). Materials and methods A radiofrequency spoiled gradient echo sequence was used to evaluate data on 19 fetuses with VM (gestational age(GA): median = 29.9 weeks (range 23 to 37.3 weeks)) and 20 healthy fetuses (GA: median = 30.9 (range 22.7 to 38.7 weeks)) at 1.5 T. Susceptibility weighted images encompassing the entire fetal brain were acquired within 1 min. An iterative, geometry constraint-based thresholded k-space division algorithm was used for generating QSM data of the fetal brain. The venous oxygen saturation was calculated using the magnetic susceptibility of the SSS obtained from the QSM data. Mixed-model analysis of variance and interobserver variability assessment were used to analyze the results. Results The median SvO2 values in the entire VM cohort as well as for second and third trimester fetuses (with interquartile range) were: 67.8% (63.2%, 73.6%), 73.1% (69.1%, 77.3%) and 63.8% (59.4%, 68.1%), respectively. The corresponding median SvO2 value in the healthy control group was: 65.3% (58.3%, 68.2%), 67.5% (61.7%, 69.2%) and 60.8% (53.6%, 68.2%), respectively. However, the difference of SvO2 between VM and control groups was not significant at the p = 0.05 level (p = 0.076). The SvO2 was found decreasing significantly with GA in the healthy control group (p Conclusions We report for the first time the estimation of cerebral SvO2 in human fetuses with VM using QSM. This measure of oxygen saturation might be beneficial in assessing and monitoring the metabolic status of the fetus in various clinical conditions.

The pathogenesis of idiopathic hypogonadotropic hypogonadism (IHH) is genetically complex. The aims of this study were to investigate the genetic profile and clinical manifestation of IHH in a Chinese pedigree and to discover new IHH-associated genes. The first step was to follow up the clinical phenotype and therapeutic outcomes of the pedigree in university hospital. The second step was that mutation screening was performed in this pedigree and 100 healthy controls. The third step was to further verify the pathogenicity of the discovered rare sequencing variant (RSV) by functional experiments. Whole exome sequencing, Sanger sequencing, testicular volume (TV), semen analysis, assessment of cell migration and necroptosis were performed. One heterozygous RSV (p.G517E) in CHL1 was identified in two male IHH patients and their mother in the pedigree, but not in healthy controls. All the three individuals exhibited olfactory impairment. hCG/hMG treatment significantly improved TV, serum testosterone and/or semen parameters of the two male patients. Functional analysis indicated that CHL1 significantly regulated GnRH neuronal cell line (GN11 cells) migration and necroptosis, with alteration of ERK1/2 activation, calcium loading, and transcription of RIPK3 and MLKL. However, the above processes were negatively influenced by the CHL1 RSV. Our study reports the genetic relevance of CHL1 in IHH, and characterizes the phenotypic and therapeutic profiles in patients carrying the CHL1 RSV. CHL1 may act as a new IHH-associated gene, and should be taken into consideration in future investigations for this field.

Isolated hypogonadotropic hypogonadism (IHH) is a rare but treatable form of male infertility caused by congenital defect in gonadotropin-releasing hormone (GnRH) secretion or action. We report a Chinese IHH male with a novel FGFR1 mutation who successfully fathered a normal son. Targeted next-generation sequencing, bioinformatics analysis and Sanger sequencing were performed by using the DNA extracted from the pedigree. The patient was treated with gonadotropin and was able to impregnant his wife during the treatment. Amniocentesis was performed at the 18 weeks of gestation. A novel de novo pathogenic missense variant (c.980A>G, p.Asn327Ser) in exon 8 in FGFR1 gene (NM_001174067.1) was identified in the patient but not in his normal parents. This variant was also absent in the DNA obtained from the amniocentesis sample. His son has normal growth and development at the age of 2 years. This is the first case of prenatal genetic diagnosis based on the genetic testing of the IHH father by combining targeted next-generation and Sanger sequencing in IHH family. We extended the mutation spectrum of FGFR1 in IHH patients. Prenatal genetic diagnosis based on the results of genetic testing of the IHH patients may be helpful in the genetic counselling for the IHH families.

INTRODUCTION AND OBJECTIVE:Erectile dysfunction (ED) is one of most common complications in men with diabetes. ED in these men occurs at early age and present with severe symptoms. Besides, PDE5i, ...

INTRODUCTION AND OBJECTIVE:As one of diabetic complications, erectile dysfunction (ED) is more frequent and causes worse response to PDE5 inhibitors compared with non-diabetic men. Corpus cavernosu...

Background Management of diabetes mellitus induced-erectile dysfunction (DMED) is challenging because of its poor responses to phosphodiesterase type 5 inhibitors. Increasingly important roles of 12-lipoxygenase (12-LOX) have been proven in diabetes mellitus. Aim To investigate 12-LOX activity and therapeutic effect of its inhibitor, baicalein (BE), on DMED. Methods Intraperitoneal streptozotocin injection was used to induce type I DM, and an apomorphine test was used to evaluate erectile function. In experiment A, we assessed 12-LOX expression alteration in the corpus cavernosum (CC) of rats with DMED of different levels of severity. In experiment B, rats with DMED were intraperitoneally injected with BE for 4 weeks, and control rats were injected with vehicles. The erectile function was tested by cavernous nerve stimulation before penile tissue was harvested. We performed Western blot, immunohistochemistry, immunofluorescence, Masson trichrome staining, and enzyme-linked immunosorbent assays to measure related proteins in CC. Main Outcome Measure The main outcome measures included rectile response, histologic examination, and expression alteration of related proteins. Results 12-LOX upregulation was associated with the progression of type I DMED. After 4 weeks treatment, compared with the DMED group, the DMED + BE group showed better erectile responses to cavernous nerve stimulation. In the DMED + BE group, significantly enhanced endothelial nitric oxide synthase/nitric oxide/cyclic guanosine monophosphate pathway, reduced 12-LOX expression, and inhibited p38 mitogen-activated protein kinase/arginase II/L-arginine pathway were showed in CC relative to the DMED group. In addition, overactivated oxidative stress and fibrosis in the DMED group were both partially ameliorated in the DMED + BE group. Clinical Implications BE may be considered as an effective therapy for DMED, but needs to be verified in future human investigations. Strengths & Limitations The role of 12-LOX and its inhibitor, BE, is firstly demonstrated in rats with type I DMED. However, the experimental data are derived from animal models with without evidences from cellular-based experiments. Conclusion 12-LOX might serve as an important factor in the pathogenesis of type I DMED. BE alleviated erectile dysfunction in rats with type I DMED probably by inhibiting 12-LOX expression, ameliorating endothelial nitric oxide synthase dysfunction, as well as suppressing oxidative stress and fibrosis.

The aim of this study was to investigate the protective effect of Polygonatum sibiricum polysaccharides (PSP) on acute kidney injury (AKI) in rats. The AKI model was established with 100 mg/kg of gentamicin (GM) intramuscularly. Six hours post-injection, rats were given intragastrically different dosages of PSP (0.25, 0.5, and 1 g/kg) for seven consecutive days. Results showed that compared with the model group, the kidney coefficient of rats decreased significantly (P

Background Congenital hypogonadotropic hypogonadism (CHH) is a genetically heterogeneous disorder characterized by absent or incomplete puberty and infertility, and heterogeneous responses are often observed during treatment. Aim To investigate the role of CHH-associated variants in patients with CHH with poor responses to human chorionic gonadotropin (hCG). Methods This retrospective study investigated 110 Chinese male patients with CHH undergoing genetic analysis and hCG treatment. CHH-associated rare sequence variants (RSVs) were identified by using a tailored next-generation sequencing panel and were interpreted in accordance with the American College of Medical Genetics and Genomics criteria. Clinical characteristics were recorded, and Kyoto Encyclopedia of Genes and Genomes analysis was conducted to assess pathways enriched in protein networks implicated in poor responses. Outcomes The outcomes include testicular volume, serum hormonal profiles, parameters of semen analysis, pathogenicity classification, and pathway enrichment. Results Among the 110 patients, 94.55% achieved normal serum testosterone and 54.55% achieved seminal spermatozoa appearance (SSA). PLXNB1, ROBO3, LHB, NRP2, CHD7, and PLXNA1 RSVs were identified in patients who had an abnormal serum testosterone level during treatment. In spermatogenesis, the number of CHH-associated RSVs was not significantly strongly associated with delayed SSA. After pathogenicity classification, pathogenic/likely pathogenic (P/LP) RSVs were identified in 30% (33/110) of patients. Patients with P/LP RSVs showed delayed SSA compared with noncarriers, and P/LP PROKR2 RSVs showed the strongest association (48, 95% CI: 34.1–61.9 months, P = .043). Enriched pathways implicated in delayed SSA included neuroactive ligand-receptor interaction; Rap1, MAPK, PI3K-Akt signaling; and regulation of actin cytoskeleton. Clinical Implications Male patients with CHH harboring P/LP PROKR2 RSVs should be aware of a high probability of poor responses to hCG; If these patients desire fertility, it might be better to recommend hCG/human menopausal gonadotropin, hCG/recombinant follicle-stimulating hormone, or pulsatile GnRH administration before treatments start or as early as possible. Strengths & Limitations Strengths are the standardized regimen and extensive follow-up (median time of 40 months). However, included patients in the study voluntarily chose hCG treatment because of the burden of drug cost and/or little fertility desire. Therefore, human menopausal gonadotropin or follicle-stimulating hormone was not added to this cohort. Our observed correlations should be further verified in patients with CHH undergoing other treatments. Conclusion Among all P/LP RSVs, P/LP PROKR2 RSVs might correlate with poor responses in CHH under hCG treatment; our study supports the pathogenicity assessment of American College of Medical Genetics and Genomics criteria in genetic counseling, to improve management of patients with CHH.

Introduction Novel therapeutic targets for diabetes-induced erectile dysfunction (DED) are urgently needed. Previous studies have proved that S100A1, a small Ca2+-binding protein, is a pluripotent regulator of cardiovascular pathophysiology. Its absence is associated with endothelial dysfunction, the central event linking cardiovascular changes in diabetes. However, the role of S100A1 in DED remains unknown. Aim To explore the effect and underlying mechanisms of S100A1 in restoring erectile function in type I diabetic rat model. Methods Diabetes was induced by intraperitoneal injection of streptozotocin and then screened by apomorphine (APO) to confirm erectile dysfunction. Rats that met the criteria of penile erection were marked as APO-positive; otherwise, the result was APO-negative. In experiment 1, S100A1 gene expression alterations in the corpus cavernosum in moderate and established stages of DED were analyzed. In experiment 2, S100A1 and control GFP gene were delivered into the corpus cavernosum in APO-negative rats by adeno-associated virus (AAV) serotype 9. Erectile function was assessed at 4 weeks after gene therapy. Main Outcome Measures Erectile response, histologic and molecular alterations. Results S100A1 protein was localized to the area surrounding the cavernosal sinusoids in the penis, and it was gradually downregulated synchronized with the progression of DED. Compared with an injection of AAV-GFP, a single injection of AAV-S100A1 significantly restored erectile function in diabetic rats. S100A1 overexpression significantly upregulated the expression of endogenous VEGF-A, promoted VEGFR2 internalization, and subsequently triggered the protein kinase B–endothelial nitric oxide synthase pathway in diabetic erectile tissues. Marked increases in nitric oxide and endothelial content were noted in AAV-S100A1-treated diabetic rats. Clinical Implications Local S100A1 overexpression may be an alternative therapy for DED and should be further investigated by future clinical studies. Strength & Limitations This is the first study demonstrating the angiogenic role of S100A1 in DED, but does not preclude the contribution of the effects of S100A1 in other tissues such as the neuronal tissue on the functional effects observed in erectile responses. Conclusion The decreased expression of S100A1 during hyperglycemia might be important in the development of erectile dysfunction. S100A1 may play a potential role in restoring erectile function in rats with DED through modulating cavernous angiogenesis.

Aim The present study compares the effect and accuracy of the superficial mark guided localization (SGL) and hook-wire guided localization (WGL) techniques for non-palpable breast microcalcifications. Methods This retrospective study was conducted to compare SGL and WGL techniques. These techniques were performed on 51 patients with non-palpable breast microcalcifications from January 2015 to May 2016. Results Among these 51 patients, 25 (49.01%) patients were subjected to WGL and 26 patients (50.99%) were subjected to SGL. The SGL technique had a higher rate of malignant cancer detection (WGL = 12.0% and SGL = 23.0%). Furthermore, no significant differences were found with regard to average age, the rate of a second excision and the diameter of the excised tissue. Moreover, no complications were observed in the SGL group, while four (16.0%) patients in the WGL group experienced problems. Conclusion The SGL technique is as accurate as the WGL technique. Furthermore, the procedure has advantages of being less expensive and causing less complications.

Objective The aim of this study was to evaluate the patient demographic and computed tomography (CT) imaging findings of spontaneous osteosarcoma in craniomaxillofacial fibrous dysplasia. Study Design Ten cases of spontaneous osteosarcoma in craniomaxillofacial fibrous dysplasia diagnosed during 1993-2013 were reviewed. Eight cases with CT images were reviewed. Results The mean age of diagnosis of osteosarcoma was 37.8 years (range, 8-55 years). The presence of a soft tissue extension component beyond the area of cortical bone destruction was demonstrated radiographically in 7 out of 8 cases. Mineralization of tumor matrix was seen in 6 cases. Periosteal reaction was demonstrated in only 1 case; 1 out of 6 cases showed significant enhancement on postcontrast CT images. Nine patients had surgical resections of tumor. Seven of them died of tumor, with a mean survival time of 5.3 years. Conclusions This study provides CT imaging features with clinical information of spontaneous osteosarcoma in craniomaxillofacial fibrous dysplasia.

Objective Today, more and more evidence suggests that Foxk proteins (Foxk1 and Foxk2) work as transcriptional repressors in different kinds of cancer, but whether Foxk1 has a role in mediating tumorigenesis in breast cancer, the evidence is rare. Methods MCF-7 cells transfected with shFoxk1 displayed a mesenchymal morphology and reduced the expression of E-cadherin, and increased the expression of N-cadherin. Transwell invasion assay and living imaging assay show that the overexpression of Foxk1 could inhibit metastasis in vitro and in vivo. Ribonucleic acid sequencing revealed that the knockdown of Foxk1 resulted in the up-regulation of different oncogenes, which was implicated in metastasis and tumor angiopoiesis. Quantitative chromatin immunoprecipitation, chromatin immunoprecipitation and Luciferase reporter assays suggested that Foxk1 could bind to the promoter of epithelial-mesenchymal transition inducer Twist and vascular endothelial growth factor, VEGF. Mass Spectrometry, co-immunoprecipitation assays and glutathione-S-transferase pull-down assay detected that Foxk1 was physically associated with Ten-eleven translocation 1, TET1, in vivo and in vitro. Results We reported that the mean expression level of Foxk1 in breast cancer was significantly lower than the adjacent noncarcinoma tissue. The higher Foxk1 expression was associated with better prognosis. Endothelial tube formation assays indicated that Foxk1 might regulate breast cancer angiogenesis through transcriptional repression of vascular endothelial growth factor. Furthermore, in vivo magnetic resonance imaging revealed the overexpression of Foxk1 could enhance the detection of the tumors. Further, a strong negative correlation was observed between Foxk1 and Twsit or between Foxk1 and vascular endothelial growth factor, and the higher Foxk1 expression is correlated with better over all survivals and better relapse-free survivals. Conclusions Together, our data indicated the function of Foxk1 as a tumor suppressor in facilitating angiogenesis and metastasis in breast cancer.

In this study, we aimed to explore the potential of dual-energy computed tomography (DECT) in evaluating liver fat; we also compared the diagnostic performance of DECT, T1-weighted dual-echo magnetic resonance (MR) imaging, and 1H-MR spectroscopy (1H-MRS) in assessing hepatic steatosis in a fatty liver rat model. Fat (water) concentration measurements by DECT spectral imaging, MR findings, and 1H-MRS measurements of hepatic fat showed similar correlations with the histopathologic results. Furthermore, a good correlation was observed between the fat (water) concentration and 1H-MRS measurements (r = 0.800 and P less than 0.001). The discriminant accuracies of the fat (water) concentration, MR findings, and 1H-MRS measurements were 66.7, 64, and 56 percent, respectively. Therefore, we conclude that the findings of DECT spectral CT imaging are strongly correlated with histopathologic findings in cases of steatosis; in addition, DECT can allow rapid, accurate evaluations of hepatic steatosis that are as effective as those obtained using T1-weighted dual-echo MR imaging and 1H-MRS.