Primary leiomyosarcoma of epididymis: a case report.

BACKGROUND: Leiomyosarcoma is a tumor that can develop in any organ that contains smooth muscles. Although leiomyosarcoma is common, its epididymal localization is quite rare. CASE PRESENTATION: A 79-year-old male Chinese Han patient presented with mild pain in the right groin and scrotum for 3 years concomitant with right scrotal swelling. Ultrasonography and magnetic resonance imaging of the scrotum showed a irregular and heterogeneous mass that was extratesticular. Right high orchiectomy was performed, and pathological examination of the resected specimen confirmed the diagnosis of leiomyosarcoma of the epididymis with surgical margins clear of tumor. CONCLUSION: Epididymal leiomyosarcoma is rare and difficult to diagnose preoperatively. The final diagnosis of epididymal leiomyosarcoma requires histologic examination. Resection must be extensive and complete. The effect of chemotherapy and radiation on the epididymal leiomyosarcoma remains unclear. Recurrence is common, so follow-up is necessary.

Bioactive 5/5/5/6 Four-Ring System Iridoids from Plumeria alba L.

Two rare 5/5/5/6 four-ring system iridoids, allamancins A and B (1 and 2) together with one known biogenetically related iridoid derivative, 3-O-methyallamancin (3) were isolated from the flowers of Plumeria alba L. The structures of these iridoid derivatives were determined by comprehensive spectroscopic analyses. The absolute configuration of 1 was confirmed by X-ray crystallographic analysis. The inhibitory activities of compounds 1-3 against nitric oxide (NO) production induced and three cancer cell lines were evaluated in vitro. Compounds 1 and 3 showed inhibitory activities on NO production with IC50 values of 18.3±0.12 and 22.1±0.14 µM, respectively. Compounds 1-3 showed moderate inhibitory activities against cancer cell lines of A549, Hela and MCF-7.

Chronic myeloid leukemia with sleep-related painful erections as a first symptom: a case report.

BACKGROUND: Sleep-related painful erections are characterized by deep penile pain that occurs during erections in the rapid eye movement stage of sleep. CASE PRESENTATION: This case presents a 43-year-old Chinese Han patient with sleep-related painful erections. Turgid painful erections (4-5 episodes of tumescence) during the sleep hours caused pain. Further, blood testing revealed an abnormal increase in white blood cells (123 × 109/L). The patient was diagnosed with chronic myeloid leukemia by bone marrow biopsy, BCR::ABL1 fusion gene testing, and Philadelphia chromosome. However, the sleep-related painful erections have dramatically decreased in frequency of erectile pain after chemotherapy for Chronic myeloid leukemia in our case. CONCLUSION: We considered that the occurrence of sleep-related painful erections was related to chronic myeloid leukemia and the case might be secondary sleep-related painful erections.

Alleviative Effect of Ruellia tuberosa L. on Insulin Resistance and Abnormal Lipid Accumulation in TNF-α-Treated FL83B Mouse Hepatocytes.

Type 2 diabetes mellitus (T2DM) is a chronic metabolic disease, and most patients with T2DM develop nonalcoholic fatty liver disease (NAFLD). Both diseases are closely linked to insulin resistance (IR). Our previous studies demonstrated that Ruellia tuberosa L. (RTL) extract significantly enhanced glucose uptake in the skeletal muscles and ameliorated hyperglycemia and IR in T2DM rats. We proposed that RTL might be via enhancing hepatic antioxidant capacity. However, the potent RTL bioactivity remains unidentified. In this study, we investigated the effects of RTL on glucose uptake, IR, and lipid accumulation in vitro to mimic the T2DM accompanied by the NAFLD paradigm. FL83B mouse hepatocytes were treated with tumor necrosis factor-α (TNF-α) to induce IR, coincubated with oleic acid (OA) to induce lipid accumulation, and then, treated with RTL fractions, fractionated with n-hexane or ethyl acetate (EA), from column chromatography, and analyzed by thin-layer chromatography. Our results showed that the ethyl acetate fraction (EAf2) from RTL significantly increased glucose uptake and suppressed lipid accumulation in TNF-α plus OA-treated FL83B cells. Western blot analysis showed that EAf2 from RTL ameliorated IR by upregulating the expression of insulin-signaling-related proteins, including protein kinase B, glucose transporter-2, and peroxisome proliferator-activated receptor alpha in TNF-α plus OA-treated FL83B cells. The results of this study suggest that EAf2 from RTL may improve hepatic glucose uptake and alleviate lipid accumulation by ameliorating and suppressing the hepatic insulin signaling and lipogenesis pathways, respectively, in hepatocytes.

[Retracted] Anticancer activity of taraxerol acetate in human glioblastoma cells and a mouse xenograft model via induction of autophagy and apoptotic cell death, cell cycle arrest and inhibition of cell migration.

Following the publication of the above paper, a concerned reader drew to the Editor's attention that several figures (Figs. 3, 4, 7 and 10) contained apparent anomalies, including repeated patternings of data within the same figure panels. Furthermore, Fig. 3 contained data that bore striking similarities to data published in Fig. 6 in another paper published in Molecular Medicine Reports, which has now been retracted [Zhu Y­Y, Huang H­Y and Wu Y­L: Anticancer and apoptotic activities of oleanolic acid are mediated through cell cycle arrest and disruption of mitochondrial membrane potential in HepG2 human hepatocellular carcinoma cells. Mol Med Rep 12: 5012­5018, 2015]. After having conducted an independent investigation in the Editorial Office, the Editor of Molecular Medicine Reports has determined that the above paper should be retracted from the Journal on account of a lack of confidence concerning the originality and the authenticity of the data. The authors were asked for an explanation to account for these concerns, but the Editorial Office never received any reply. The Editor regrets any inconvenience that has been caused to the readership of the Journal. [the original article was published in Molecular Medicine Reports 13: 4541­4548, 2016; DOI: 10.3892/mmr.2016.5105].

LncRNA BLACAT1 is involved in chemoresistance of non­small cell lung cancer cells by regulating autophagy.

The aim of the present study was to determine the effect of the long non­coding RNA (lncRNA) bladder cancer­associated transcript 1 (BLACAT1) in chemoresistance of non­small cell lung cancer (NSCLC) cells. Expression of lncRNA BLACAT1, microRNA (miR)­17, autophagy­related protein 7 (ATG7), multidrug­resistance protein 1 (MRP1), and the autophagy­associated proteins light chain 3 (LC3)­II/LC3­I and Beclin 1 were detected using the reverse transcription­quantitative polymerase chain reaction and western blot analysis. Cell viability was determined using an MTT assay. The interaction between BLACAT1 and miR­17 was determined using RNA immunoprecipitation and RNA pull­down assays. A cisplatin (DDP)­resistant NSCLC cell A549/DDP xenograft model in nude mice was established to investigate the effect of BLACAT1 on the chemoresistance of NSCLC cells. Compared with in DDP­sensitive NSCLC cells, expression of BLACAT1, ATG7, MRP1, LC3­II/LC3­I and Beclin 1 was significantly upregulated in DDP­resistant NSCLC cells, whereas miR­17 was downregulated in DDP­resistant NSCLC cells. Short interfering RNA against BLACAT1 decreased the viability of DDP­resistant NSCLC cells. In addition, BLACAT1 interacted with miR­17, and negatively regulated miR­17. BLACAT1 promoted ATG7 expression through miR­17, and facilitated autophagy and promoted chemoresistance of NSCLC cells through miR­17/ATG7. Finally, in vivo experiments indicated that inhibition of BLACAT1 ameliorated the chemoresistance of NSCLC. BLACAT1 was upregulated in DDP­resistant NSCLC cells, and promoted autophagy and chemoresistance of NSCLC cells through the miR­17/ATG7 signaling pathway.

Suppression of microRNA-130b inhibits glioma cell proliferation and invasion, and induces apoptosis by PTEN/AKT signaling.

Glioblastoma is the most common malignant brain tumor in adults and is characterized by extensive proliferation and the diffused invasion of tumor cells. Due to the intricate signaling pathways involved in glioma progression, more effective targeted therapies and prognostic biomarkers in clinical practice are required. The suppression of proto-oncogene function or recovery of tumor suppressor gene function remains one of the primary approaches in gene therapy. The close association between the abnormal expression or mutation of microRNA (miRNA) and the tumorigenesis, progression and staging in glioma have been demonstrated previously. However, the expression pattern and specific role of microRNA­130b (miR­130b) in the tumor occurrence and progression of glioma are unclear. In the present study, quantitative polymerase chain reaction was performed to determine the expression level of miR-130b in 30 brain glioma patients and 3 glioma cell lines. An miR­130b inhibitor was transfected into U87 cells to downregulate the expression of miR-130b, and assessments of cell proliferation, cell cycle, apoptosis, cell invasion and migration in vitro and nude mouse tumorigenicity in vivo were conducted. Western blotting and luciferase reporter gene technology were used to verify the downstream target gene of miR-130b, namely phosphatase and tensin homolog (PTEN). The results demonstrated that miR-130b expression was increased in glioma tissues and cell lines in comparison with non-glioma tissues or cells. The downregulated expression of miR-130b inhibited the proliferation and invasion of glioma cells, induced apoptosis of the cells in vitro and inhibited their tumorigenicity in vivo. Western blotting and luciferase reporter assays demonstrated that the PTEN gene is a direct target of miR­130b. Western blotting revealed that the miR-130b inhibitor upregulated the expression of PTEN, inhibited AKT pathway activation, upregulated the tumor suppressor gene p27, and suppressed cyclin D1, matrix metalloproteinase 2 and 9 expression. These results suggest that the miR-130b inhibitor suppressed glioma cell proliferation and invasion via the PTEN/AKT pathway. Therefore, miR­130b is suggested to be an effective therapeutic target for glioma.

Anticancer activity of taraxerol acetate in human glioblastoma cells and a mouse xenograft model via induction of autophagy and apoptotic cell death, cell cycle arrest and inhibition of cell migration.

The aim of the present study was to investigate the in vitro and in vivo anticancer and apoptotic effects of taraxerol acetate in U87 human glioblastoma cells. The effects on cell cycle phase distribution, cell cycle-associated proteins, autophagy, DNA fragmentation and cell migration were assessed. Cell viability was determined using the MTT assay, and phase contrast and fluorescence microscopy was utilized to determine the viability and apoptotic morphological features of the U87 cells. Flow cytometry using propidium iodide and Annexin V-fluorescein isothiocyanate demonstrated the effect of taraxerol acetate on the cell cycle phase distribution and apoptosis induction. Western blot analysis was performed to investigate the effect of the taraxerol acetate on cell cycle­associated proteins and autophagy­linked LC3B­II proteins. The results demonstrated that taraxerol acetate induced dose­ and time­dependent cytotoxic effects in the U87 cells. Apoptotic induction following taraxerol acetate treatment was observed and the percentage of apoptotic cells increased from 7.3% in the control cells, to 16.1, 44.1 and 76.7% in the 10, 50 and 150 µM taraxerol acetate­treated cells, respectively. Furthermore, taraxerol acetate treatment led to sub­G1 cell cycle arrest with a corresponding decrease in the number of S­phase cells. DNA fragments were observed as a result of the gel electrophoresis experiment following taraxerol acetate treatment. To investigate the inhibitory effects of taraxerol acetate on the migration of U87 cell, a wound healing assay was conducted. The number of cells that migrated to the scratched area decreased significantly following treatment with taraxerol acetate. In addition, taraxerol acetate inhibited tumor growth in a mouse xenograft model. Administration of 0.25 and 0.75 µg/g taraxerol acetate reduced the tumor weight from 1.2 g in the phosphate­buffered saline (PBS)­treated group (control) to 0.81 and 0.42 g, respectively. Similarly, 0.25 and 0.75 µg/g taraxerol acetate injection reduced the tumor volume from 1.3 cm3 in the PBS-treated group (control) to 0.67 and 0.25 cm3, respectively.

MicroRNA-130b promotes cell proliferation and invasion by inhibiting peroxisome proliferator-activated receptor-γ in human glioma cells.

MicroRNA-130b (miR-130b) is a novel tumor-related miRNA that has been found to be involved in several biological processes. However, there is limited evidence regarding the role of miR-130b in the tumorigenesis of human gliomas. In the present study, reverse transcription-quantitative polymerase chain reaction (RT-qPCR) assays were used to quantify miR-130b expression levels in human glioma tissues and glioma cell lines (U251, U87, SNB19 and LN229). The expression level of miR-130b was found to be markedly higher in human glioma tissues than in non­neoplastic brain specimens. Specifically, higher expression levels of miR­130b were observed in the glioma cell lines, compared with those in normal human astrocytes (NHA). We also confirmed that miR­130b interacted with the 3'-untranslated region of peroxisome proliferator­activated receptor-γ (PPAR­Î³), which negatively affected the protein levels of E-cadherin. Furthermore, its effects on cell proliferation and invasion were examined using CCK8, colony formation, cell cycle and Transwell assays. We found that the upregulation of miR-130b induced cell proliferation, decreased the percentage of cells in the G0/G1 phase and enhanced the invasiveness of U251 glioma cells whereas the downregulation of miR-130b exerted opposing effects. Moreover, it was demonstrated that the downregulation of miR­130b in U251 glioma cells restored the expression of PPAR-γ and E-cadherin, and inhibited the expression of ß-catenin. Notably, PPAR-γ knockdown abolished the inhibitory effect of miR-130b inhibitor on the proliferation and invasivness of U251 cells. Taken together, these findings suggest that miR­130b promotes the proliferation and invasion of U251 glioma cells by inhibiting PPAR-γ.

TPX2 promotes glioma cell proliferation and invasion via activation of the AKT signaling pathway.

Glioblastoma multiforme (GBM) is the most common and most malignant type of primary adult brain cancer. The most common phenotype associated with GBM is cellular invasion; however, the molecular mechanisms governing this process are poorly understood. Targeting protein for Xenopus kinesin-like protein 2 (TPX2) is a nuclear protein with roles in cellular proliferation and mitotic spindle assembly. TPX2 is overexpressed in various malignancies, including human malignant astrocytoma. Despite this finding, the exact role of TPX2 in human glioma is not well defined. The present study reports the elevated expression of TPX2 in a number of glioma cell lines. TPX2 overexpression promoted cellular proliferation, decreased the percentage of cells in G0/G1 phase, and increased invasion of both U251 and U87 cells. Overexpression of TPX2 also significantly enhanced the phosphorylation of AKT, decreased the expression of p21, and increased the expression of cyclin D1 and matrix metallopeptidase (MMP)-9. In both U251 and U87 cells, knockdown of TPX2 resulted in phenotypes that are in direct contrast to those observed following TPX2 overexpression. Specifically, TPX2 knockdown inhibited cell proliferation, increased the percentage of cells in G0/G1 phase, inhibited invasion, decreased AKT phosphorylation, decreased the expression of MMP-9 and cyclin D1, and increased p21 expression. The AKT inhibitor IV in large part phenocopied the effect of TPX2 knockdown. The present data suggest that TPX2 promotes glioma cell proliferation and invasion via AKT signaling.

Ligand free copper(I)-catalyzed synthesis of diaryl ether with Cs2CO3 via a free radical path.

Complexes [Cu(I)(2,4-dimethylphenoxy)2](-) (A) and [Cu(II)(2,4-dimethylphenoxy)2(p-tolyl)](-) (B) were observed by in situ electrospray ionization mass spectrometry (ESI-MS) analysis of the ligand free copper(I)-catalyzed C-O coupling reaction using Cs2CO3 under the catalytic reaction conditions indicating that they could be intermediates in the reaction. The radical scavenger cumene retarded the reaction. Catalytic cycles involving a free radical path are proposed based on these observations.

Clinical application of anatomy landmarks for microscopic endonasal transsphenoidal surgery for pituitary adenomas.

It is important to identify relevant anatomical landmarks on the route of endonasal transsphenoidal surgery (TSS) for pituitary adenomas to improve the gross total resection and the remission of disease. We therefore retrospectively studied the clinical outcomes of 148 patients who underwent single nostril endonasal TSS for pituitary adenomas. The anatomic basis of these procedures was evaluated. The important landmarks included the mucosal sphenoid ostia, the sphenoid keel, the osseous ostia and the nutrient arteries nearby, the sellar bulge, and the carotid protuberance, which outlined a clear route to the sella turcica with the best view and less tissue damage. Based on these landmarks, 148 cases of endonasal TSS were successfully performed to achieve 70.3% of gross total resection and remission, respectively. The complications were controlled to the least. Therefore, the application of these landmarks will help to prevent complications and improve the long-term outcomes.

Value of anatomical landmarks in single-nostril endonasal transnasal-sphenoidal surgery.

The sphenoid sinus occupies a central location in transsphenoidal surgery (TSS). It is important to identify relevant anatomical landmarks to enter the sphenoid sinus and sellar region properly. The aim of this study was to identify anatomical landmarks and their value in single-nostril endonasal TSS. A retrospective study was performed to review 148 cases of single-nostril endonasal TSS for pituitary lesions. The structure of the nasal cavities and sphenoid sinus, the position of apertures of the sphenoid sinus and relevant arteries and the morphological characteristics of the anterior wall of the sphenoid sinus and sellar floor were observed and recorded. The important anatomical landmarks included the mucosal aperture of the sphenoid sinus, a blunt longitudinal prominence on the posterior nasal septum, the osseocartilaginous junction of the nasal septum, the 'bow sign' of the anterior wall of the sphenoid sinus, the osseous aperture and its relationship with the nutrient arteries, the bulge of the sellar floor and the carotid protuberance. These landmarks outlined a clear route to the sella turcica with an optimal view and lesser tissue damage. Although morphological variation may exist, the position of these landmarks was generally consistent. Locating the sphenoid sinus aperture is the gold standard to direct the surgical route of TSS. The 'bow sign' and the sellar bulge are critical landmarks for accurate entry into the sphenoid sinus and sella fossa, respectively.

EPHX1 A139G polymorphism and lung cancer risk: a meta-analysis.

Microsomal epoxide hydrolase 1 (EPHX1) plays an important role in both the activation and the detoxification of polycyclic aromatic hydrocarbons and aromatic amines. Polymorphisms at exon 4 of the EPHX1 gene have been reported to be associated with variations in EPHX1 activity. Many studies have investigated the association between EPHX1 A139G polymorphism and lung cancer risk, but the impact of EPHX1 A139G polymorphism on lung cancer risk is not clear owing to the apparent inconsistence among those studies. This study aimed to identify the association between EPHX1 A139G polymorphism and lung cancer risk by performing a meta-analysis. We used the pooled odds ratio (OR) with its corresponding 95 % confidence interval (95 % CI) to explore the association. Finally, 26 studies with a total of 14,494 subjects were included into this meta-analysis. Meta-analyses of total studies showed the EPHX1 A139G polymorphism was associated with lung cancer risk under three genetic models (OR (G versus A) = 1.17, 95 % CI 1.04-1.31, P (OR) = 0.01; OR (AG versus AA) = 1.21, 95 % CI 1.06-1.37, P (OR) = 0.004; OR (AG + GG versus AA) = 1.22, 95 % CI 1.06-1.39, P (OR) = 0.005). Sensitivity analyses and subgroup analyses further identified the significant association between the EPHX1 A139G polymorphism and lung cancer risk. No evidence of publication bias was observed. Meta-analyses of available data supported the concept of EPHX1 A139G polymorphism as a genetic susceptibility factor for lung cancer.

The effect of galectin-3 genetic variants on the susceptibility and prognosis of gliomas in a Chinese population.

The aim of this study is to explore the association between the polymorphisms of galectin-3 gene and clinico-pathological characteristics and prognosis of gliomas. We enrolled 190 histologically diagnosed gliomas and 210 healthy controls in this study. Two genetic variants at galectin-3 single nucleotide polymorphism (SNP) sites (galectin-3 +191 A>C and +292 A>C) were determined. We found that the A/A genotype at galectin-3 gene +292 A>C was significantly more prevalent in gliomas patient than in controls (42.1% vs. 29.0%, P=0.021); the A allele frequency was markedly higher in gliomas subjects than in controls (61.8% vs. 45.0%, P=0.008). There was a markedly higher prevalence of AA carriers in high-grade subgroup than in low-grade subgroup (50.5% vs. 31.8%, P=0.012). The Kaplan-Meier analyses showed that the gliomas patients carrying AA genotype of galectin-3 gene +292 A>C had marked shorter overall survival period than those did not (AA vs. AC+CC, 22.2±3.8 months vs. 38.3 months±7.9; P=0.04). The SNPs at +191 A>C of galectin-3 gene did not show positive association with clinico-pathological characteristics and prognosis of gliomas. The results of this study suggest the SNPs at +292 A>C, not SNPs at +191 A>C, of galectin-3 gene were associated with the tumor grade and prognosis of gliomas.

[Dutasteride in the treatment of benign prostatic hyperplasia: an update].

Benign prostatic hyperplasia (BPH) is a common disease in older men. At present, 5alpha reductase inhibitor-based medication, preferred by most BPH patients as the first-choice therapy, is taking place of traditional transurethral resection of the prostate. This article presents an update of the researches on the treatment of BPH with dutasteride--a novel 5 alpha-reductase inhibitor.