Low-dose CT of paediatric paranasal sinus using an ultra-low tube voltage (70 kVp) combined with the flash technique.

AIM: To evaluate the radiation dose and diagnostic image quality of low-dose computed tomography (CT) of the paranasal sinus in children, with acquisition at an ultra-low tube voltage (70 kVp) combined with the Flash technique. MATERIALS AND METHODS: Eighty paediatric patients underwent CT of the paranasal sinus and were divided into two groups according to different protocols (group A: 80 kVp protocol with conventional spiral mode [n=40] and group B: 70 kVp protocol with Flash scan mode [n=40]). For each examination, the CT dose index (CTDIvol), dose-length product (DLP), and effective dose (ED) were estimated. The image noise, signal-to-noise ratio (SNR), and overall subjective diagnostic image quality were also evaluated. RESULTS: For radiation dose, the CTDIvol (mGy), DLP (mGy·cm), and ED (mSv) values of the 70 kVp protocol were significantly lower than those of the 80 kVp protocol (CTDIvol: 1.57±0.009 versus 0.39±0.004 mGy, p<0.001; DLP: 19.88±2.01 versus 6.31±0.52 mGy·cm, p<0.001; ED: 0.079±0.016 versus 0.024±0.005 mSv, p<0.001). Compared with those of the 80-kVp protocol, the image noise increased by 40.7% (p=0.113), the SNRsoft-tissue decreased by 48.9%, and the SNRbone increased by 10.1% with the 70-kVp protocol (p=0.176 and 0.227, respectively). There was no significant difference in the overall subjective image quality grades between these two groups (p=0.15). CONCLUSION: When imaging the paranasal sinus in children, an ultra-low tube voltage (70 kVp) combined with the Flash CT technique can reduce the radiation dose significantly while maintaining diagnostic image quality with clinically acceptable image noise.

MiRNA-206 inhibits proliferation of renal clear cell carcinoma by targeting ZEB2.

OBJECTIVE: The purpose of this study was to investigate the effect of microRNA-206 on the malignant progression of renal clear cell carcinoma (RCC). In addition, whether microRNA-206 could regulate ZEB2 expression and the underlying mechanisms was also explored. PATIENTS AND METHODS: Quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) was performed to examine microRNA-206 level in 46 tumor tissue specimens and adjacent ones of RCC patients. Also, the relationship between microRNA-206 expression and clinical indicators of RCC was analyzed. The negative control (NC) and microRNA-206 mimics were transfected into RCC cell lines, and the transfection efficiency was verified by qRT-PCR. The effects of microRNA-206 on the proliferation and apoptosis of RCC cells were analyzed by cell counting kit-8 (CCK-8), clone formation, and flow cytometry assays. Finally, the regulation of microRNA-206 on the downstream gene ZEB2 was indicated by Western Blot and cell recovery experiments. RESULTS: qRT-PCR results showed that the expression level of microRNA-206 in tumor tissue samples of RCC patients was remarkably lower than that in adjacent normal tissues, and the difference was statistically significant. Meanwhile, compared with patients with high expression of microRNA-206, the pathological stage of patients with low expression of microRNA-206 was higher, and the overall survival rate was lower. In the RCC cell lines (Caki-1 and Caki-2), the cell proliferation ability of the microRNA-206 overexpression group was remarkably weakened, while the cell apoptosis rate was oppositely enhanced when compared with the NC group. In addition, this study demonstrated that ZEB2 expression was remarkably increased in RCC cells as well as tissues and was negatively correlated with microRNA-206 expression. At the same time, microRNA-206 mimics was found remarkably reduced in the expression of proteins in ZEB2-related signaling pathway, including ZEB2, ß-catenin, cyclinD1, c-Myc, MMP-2, and MMP-9. In the cell reverse experiment, the overexpression of ZEB2 was found to be able to counteract the impact of microRNA-206 mimics on RCC cell proliferation and apoptosis and thus, participated in the malignant progression of RCC. CONCLUSIONS: This study revealed that microRNA-206 was remarkably associated with the pathological stage and poor prognosis of RCC patients. In addition, microRNA-206 might inhibit the malignant progression of RCC by regulating the targeted ZEB2.

MiRNA-1179 suppresses the metastasis of hepatocellular carcinoma by interacting with ZEB2.

OBJECTIVE: To investigate the biological function of microRNA-1179 (miRNA-1179) in regulating the proliferative and migratory abilities of the hepatocellular carcinoma (HCC) by targeting zinc-finger E-box-binding homeobox 2 (ZEB2). PATIENTS AND METHODS: The miRNA-1179 level in 40 HCC tissues and matched normal tissues was detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). The association between the miRNA-1179 level and the clinical parameters of HCC patients was analyzed. The regulatory effects of miRNA-1179 on influencing proliferative and migratory abilities of HepG2 and Bel-7402 cells were assessed. The dual-luciferase reporter gene assay was conducted to verify the binding relationship between miRNA-1179 and ZEB2. Subsequently, the expression pattern and the biological function of ZEB2 in HCC were explored. The rescue experiments were finally carried out to uncover the role of the miRNA-1179/ZEB2 axis in regulating the progression of HCC. RESULTS: MiRNA-1179 was downregulated in HCC tissues and cell lines. HCC patients with low expression of miRNA-1179 had higher metastatic rates (lymphatic metastasis and distant metastasis) and worse prognosis relative to those with low expression. The overexpression of miRNA-1179 attenuated the proliferative and migratory abilities of HCC cells. ZEB2 was confirmed to be the direct target of miRNA-1179 and its level was negatively regulated by miRNA-1179. ZEB2 was upregulated in HCC tissues and cell lines. The high expression of ZEB2 predicted a worse prognosis of HCC. The overexpression of ZEB2 reversed the inhibitory effects of miRNA-1179 on the proliferative and migratory abilities in HCC cells. CONCLUSIONS: MiRNA-1179 is closely related to lymphatic metastasis, distant metastasis, and overall survival of HCC. It alleviates the malignant progression of HCC by downregulating ZEB2.

Screening of parathyroid gland by high frequency ultrasound and the relationship between recurrent urinary calculi and primary hyperparathyroidism.

OBJECTIVE: To understand the value of high frequency ultrasound in the clinical screening of parathyroid gland, and to summarize the intrinsic relationship between primary hyperparathyroidism and recurrent urinary calculi. PATIENTS AND METHODS: 98 cases of urinary calculi were randomly selected, and the patients were admitted to our hospital from March 2014 to August 2017. A total of 100 healthy subjects were selected as group B in the same period. High frequency color Doppler ultrasonography scan recorded the results. RESULTS: Among the subjects in group A, 67 (68.37%) showed parathyroid gland, 14 cases (14.29%) had tumor mass in the parathyroid system, 40 cases more than those in group B (40.00%) and 2 cases (2.00%), (p <0.05). There were 10 cases (10.20%) of primary hyperparathyroidism in group A and no cases of primary hyperparathyroidism in group B (p < 0.05). The occurrence of primary hyperparathyroidism was 26.92% (7/26) in the number of cases, with 3 and more cases of urinary calculi, which was higher than that in the first recurrent cases (3/72), (p<0.005). CONCLUSIONS: One of the key causes of recurrent episodes of urinary calculi is primary hyperparathyroidism, which can be applied to high frequency ultrasonography to develop professional screening of parathyroid gland in cases of urinary calculi.

LncRNA SNHG7 promotes the proliferation of esophageal cancer cells and inhibits its apoptosis.

OBJECTIVE: Our research studied the expression of long noncoding RNA (lncRNA) SNHG7 in esophageal cancer cells and tissues. The effect of lncRNA SNHG7 on proliferation and apoptosis of esophageal cancer cells has been discussed. PATIENTS AND METHODS: Si-SNHG7 was transfected into esophageal cancer cells, and qRT-PCR was performed to detect the expression of lncRNA SNHG7 in esophageal cancer cells and tissues. The effect of SNHG7 on the proliferation of esophageal cancer cells was measured by CCK8 assay and plate cloning assay, respectively. Flow cytometry was used to detect the effect of SNHG7 on the cell cycle and apoptosis rate of esophageal cancer cells. Changes in expression of downstream protein p15 and p16 after si-SNHG7 intervention were analyzed by qRT-PCR and Western blot. RESULTS: QRT-PCR showed that the expression of SNHG7 in esophageal cancer tissues and cells was significantly up-regulated. After the si-SNHG7 intervention, the proliferation of esophageal cancer cells was inhibited, the apoptosis rate increased, and the cell cycle was blocked in G1-G0 phase. QRT-PCR and Western blot showed that, after the si-SNHG7 intervention, the expression of p15 and p16 increased significantly. CONCLUSIONS: The expression of SNHG7 in the tissues and cells of esophageal cancer is significantly up-regulated. SNHG7 can partly promote the development of esophageal cancer by regulating the expression of p15 and p16.

Long non-coding RNA DUXAP8 regulates proliferation and invasion of esophageal squamous cell cancer.

OBJECTIVE: The purpose of this research was to detect the expression of long non-coding RNA DUXAP8 in esophageal cancer, and to explore its underlying mechanism in the development of esophageal squamous cell carcinoma (ESCC). PATIENTS AND METHODS: We collected 78 pairs of esophageal cancer tissues and normal adjacent tissues. The mRNA level of DUXAP8 in these esophageal cancer tissues and corresponding adjacent tissues was detected by quantitative Real-time polymerase chain reaction (qRT-PCR). The relationship between DUXAP8 expression and the prognosis of esophageal cancer was analyzed. Small interfering RNA (siRNA) was applied to reduce the expression of DUXAP8 in ESCC cell lines (TE-1 and KYSE520). Meanwhile, the specific effect of DUXAP8 on the biological functions of ESCC cells was analyzed by CCK-8 assay (cell counting kit-8), colony formation assay and transwell assay, respectively. Furthermore, the regulatory effect of DUXAP8 on Wnt/ß-catenin pathway was detected by Western blot. RESULTS: DUXAP8 was overexpressed in ESCC tissues than that of normal adjacent tissues. DUXAP8 expression was positively correlated to tumor stage and lymph node metastasis, whereas negatively correlated to the survival rate of ESCC patients. Cell proliferation, colony formation and invasion abilities were significantly decreased after knockdown of DUXAP8 in ESCC cells. Western blot results showed that DUXAP8 could regulate the occurrence of ESCC via Wnt/ß-catenin pathway. CONCLUSIONS: DUXAP8 expression was significantly correlated with tumor stage, lymph node metastasis and poor prognosis of ESCC patients. DUXAP8 may promote the occurrence of ESCC via Wnt/ß-catenin pathway.

Study on the distribution of CD8+ memory T cell subsets and IFN-γ level during the spontaneous clearance of hepatitis B virus in patients with chronic hepatitis B virus infection.

OBJECTIVE: To study the alteration of CD8+ memory T cell subsets under different immune statuses during the spontaneous clearance of hepatitis B virus (HBV) in Chinese patients with chronic HBV infection. PATIENTS AND METHODS: We analyzed Chinese patients with chronic HBV infection including 10 patients with Hepatitis B surface Antigen (HBsAg) spontaneous seroconversion, 25 patients with Hepatitis B virus e Antigen (HBeAg) spontaneous seroconversion, 25 patients with chronic hepatitis B (CHB), and 25 chronic HBV carriers. The CD8+ T cells in peripheral blood were isolated, and flow cytometry was used to determine the percent change of CD8+ T memory cell subsets. ELISA was used to measure the levels of Interferon-γ (IFN-γ) secretion from CD8+ T cells. RESULTS: (1) The percentage of CD8+ TN cells in peripheral blood was lower in the HBsAg seroconversion group than in the HBeAg seroconversion group (p<0.01), and higher in the CHB group and chronic HBV carrier group (p<0.01, 0.01); (2) The percentage of CD8+ TEM-2 memory T cells in peripheral blood was higher in the HBsAg seroconversion group than the HBeAg seroconversion group (p<0.05), CHB group, and chronic HBV carrier group (p<0.01, 0.01); (3) The percentage of CD8+ TEM-1 and CD8+ TCM cells in peripheral blood was higher in the CHB group and HBV carrier group than the HBsAg seroconversion group and HBeAg group, but there were no significant differences between groups (p>0.05); (4) IFN-γ production from CD8+ T cells in peripheral blood was higher in the HBsAg seroconversion group than the HBeAg seroconversion group (p<0.05), CHB group, and chronic HBV carrier group (p<0.05, 0.01). CONCLUSIONS: The consistent increase of CD8+ TEM-2 cell subsets may be an important cause of spontaneous clearance of HBV. The disorder of CD8+ memory T cell differentiation may be an important mechanism of chronic HBV infection.

Effect of Triptolide on retinal ganglion cell survival in an optic nerve crush model.

Optic nerve crush model could be used to investigate the mechanism of neuronal survival and axonal regeneration in central nervous system. Triptolide, a Chinese herb extract with anti-inflammatory and immunosuppressive activities, has shown neuron protective functions in nervous system. In this study, we investigated the changes in retinal ganglion cell survival and axonal regeneration after administration of triptolide in optic nerve crush model. Triptolide treatment tended to promote retinal ganglion cell survival rather than optic nerve regeneration as well as inhibit the expression of tumor necrosis factor-α and activation of nuclear factor-kappa B. These findings suggested that intraperitoneal injection of triptolide may be an effective treatment for optic nerve injury and this effect was attributed at least in part to its anti-inflammatory actions.

Epigenomic elements analyses for promoters identify ESRRG as a new susceptibility gene for obesity-related traits.

OBJECTIVES: With ENCODE epigenomic data and results from published genome-wide association studies (GWASs), we aimed to find regulatory signatures of obesity genes and discover novel susceptibility genes. METHODS: Obesity genes were obtained from public GWAS databases and their promoters were annotated based on the regulatory element information. Significantly enriched or depleted epigenomic elements in the promoters of obesity genes were evaluated and all human genes were then prioritized according to the existence of the selected elements to predict new candidate genes. Top-ranked genes were subsequently applied to validate their associations with obesity-related traits in three independent in-house GWAS samples. RESULTS: We identified RAD21 and EZH2 as over-represented, and STAT2 (signal transducer and activator of transcription 2) and IRF3 (interferon regulatory transcription factor 3) as depleted transcription factors. Histone modification of H3K9me3 and chromatin state segmentation of 'poised promoter' and 'repressed' were over-represented. All genes were prioritized and we selected the top five genes for validation at the population level. Combining results from the three GWAS samples, rs7522101 in ESRRG (estrogen-related receptor-γ) remained significantly associated with body mass index after multiple testing corrections (P=7.25 × 10(-5)). It was also associated with ß-cell function (P=1.99 × 10(-3)) and fasting glucose level (P<0.05) in the meta-analyses of glucose and insulin-related traits consortium (MAGIC) data set.Cnoclusions:In summary, we identified epigenomic characteristics for obesity genes and suggested ESRRG as a novel obesity-susceptibility gene.

Histamine H4 Receptor mediates interleukin-8 and TNF-α release in human mast cells via multiple signaling pathways.

Histamine, mainly produced by mast cells, is an important inflammatory mediator in immune response. Recently Histamine H4 Receptor (H4R) was also identified in mast cells, from which pro-inflammatory cytokines and chemokines are released. However, the mechanism of how H4R mediates these cytokines and chemokines release in mast cells was still unclear. To further explore the role of H4R in the immune inflammatory response in mast cells, we tested the release of inflammatory cytokine tumor necrosis factor-α (TNF-α), chemokine interleukin-8 (IL-8) and the relevant signaling pathways activated by H4R on LAD2 cells (a human mast cell line). We found that the release of IL-8 and TNF-α were blocked by inhibitors of PI3K, ERK and Ca2+-Calcineurin-NFAT signaling pathways, while the release of these cytokines and chemokines were enhanced by the inhibitor of P38 signaling pathway. However, inhibitors of the JNK and NF-κB signaling pathways had little effect on the expression of the pro-inflammatory mediators. Moreover, activation of the H4R could induce phosphorylation of ERK, p38 and AKT in mast cells. In conclusion, we found that H4R mediates the release of inflammatory cytokine TNF-α and chemokine IL-8 in human mast cells via PI3K, Ca2+-Calcineurin-NFAT and MAPKs signaling pathways.

Body girdle reduced fat deposition and altered other body parameters in rats.

Many women favor in wearing foundation garments to shape their body and show satisfactory figures. However, few investigations have been conducted on the physiological impact of wearing tight garments on the body. In this study, we used girdled rats that were fed with a high fat diet to investigate their physiological condition including alterations in food intake, body weight, fat deposition, and hormone concentrations. Over the experiment period, girdled rats maintained normal plasma and liver cholesterol and triglyceride. Leptin level in girdled rats was significantly lower than that in normal control. The fat tissue of girdled rats was more active in secretion of leptin, which might be mediated by mTOR signaling. Girdled rats showed no difference in hematology analysis during the experiment period. This study showed that a body girdle can significantly reduce fat deposition and alter other body parameters in rats.

Oleic acid-induced hepatic steatosis is coupled with downregulation of aquaporin 3 and upregulation of aquaporin 9 via activation of p38 signaling.

Excess lipid deposition in hepatocytes is a hallmark feature of nonalcoholic fatty liver disease (NAFLD). The present study was designed to explore the expression and regulation of aquaporin (AQP) 3 and AQP9 in oleic acid-induced hepatic steatosis. HepG2 cells were incubated with oleic acid at different concentrations and time points. Oil-Red-O staining and triglyceride content measurement were done to assess the extent of hepatic steatosis. The expression of AQP3 and AQP9 was assessed using quantitative real-time PCR and Western blot analyses. The mitogen-activated protein kinase (MAPK) pathways involved in the regulation of AQP3 and AQP9 expression were checked. Compared to untreated control cells, oleic acid treatment significantly (p<0.05) induced hepatic steatosis in HepG2 cells in a dose- and time-dependent fashion. Oleic acid-treated cells showed a significant reduction in the AQP3 expression and a concomitant increase in the AQP9 expression. Oleic acid exposure led to enhanced phosphorylation of p38, but not ERK1/2 or JNK MAPK. Pharmacological inhibition of p38 rather than ERK1/2 signaling significantly blocked the regulation of AQP3 and AQP9 expression by oleic acid. Oleic acid-induced hepatic steatosis in HepG2 cells is associated with the coordinated regulation of AQP3 and AQP9 via activation of p38 signaling. These findings warrant functional studies of aquaglyceroporins in NAFLD.

Predicting hepatic steatosis and liver fat content in obese children based on biochemical parameters and anthropometry.

BACKGROUND: Predictors of quantitative evaluation of hepatic steatosis and liver fat content (LFC) using clinical and laboratory variables available in the general practice in the obese children are poorly identified. OBJECTIVE: To build predictive models of hepatic steatosis and LFC in obese children based on biochemical parameters and anthropometry. METHODS: Hepatic steatosis and LFC were determined using proton magnetic resonance spectroscopy in 171 obese children aged 5.5-18.0 years. Routine clinical and laboratory parameters were also measured in all subjects. Group analysis, univariable correlation analysis, and multivariate logistic and linear regression analysis were used to develop a liver fat score to identify hepatic steatosis and a liver fat equation to predict LFC in each subject. RESULTS: The predictive model of hepatic steatosis in our participants based on waist circumference and alanine aminotransferase had an area under the receiver operating characteristic curve of 0.959 (95% confidence interval: 0.927-0.990). The optimal cut-off value of 0.525 for determining hepatic steatosis had sensitivity of 93% and specificity of 90%. A liver fat equation was also developed based on the same parameters of hepatic steatosis liver fat score, which would be used to calculate the LFC in each individual. CONCLUSIONS: The liver fat score and liver fat equation, consisting of routinely available variables, may help paediatricians to accurately determine hepatic steatosis and LFC in clinical practice, but external validation is needed before it can be employed for this purpose.

Efficacy of intratumoral chemotherapy using arsenic trioxide (As2O3) sustained release tablets for the treatment of neurogliocytoma in nude mice.

OBJECTIVE: This study aimed to investigate the inhibiting effect of arsenic trioxide (As2O3) on neurogliocytoma in nude mice and the mechanism responsible for this effect. MATERIALS AND METHODS: Neurogliocytoma implantation models were constructed in nude mice, which were assigned to three groups: the control group, the sustained release tablet-polylactic acid-glycolic acid polymer (50:50) group (PLGA group) and the As2O3-polylactic acid-glycolic acid polymer (50:50) (As2O3-PLGA group). One tablet of As2O3-PLGA was implanted in the tumor of the As2O3-PLGA group. Intratumoral implantation was also performed in the other groups using a different type of tablet. The sustained releasing As2O3 had an inhibiting effect on the tumors. The TUNEL assay was used to determine the apoptosis rates in the implanted tumors. Immunohistochemical staining and Western blotting was carried out to determine the expression levels of caspase-3 and Bcl-2. RESULTS: No inhibitory effect was observed on the tumor in the PLGA group, and there was no significant difference between this group and the control group. Subcutaneous tumor growth in nude mice was significantly inhibited in the As2O3-PLGA group relative to that in the control group, and the difference was statistically significant (p < 0.01). The tumor inhibition rate was 60.8%. The percentage of apoptotic tumor cells in the As2O3-PLGA group was 30.8%, which was significantly higher than that in the control group (3.92%) and that in the PLGA group (4.08%). The expression of Bcl-2 in the implanted tumor tissue was significantly reduced, but the expression of caspase-3 increased significantly. CONCLUSIONS: As2O3 has a potent inhibiting effect on the growth of neurogliocytoma in vivo and can induce the apoptosis of tumor cells. The molecular mechanism of this effect may be related to the downregulation of Bcl-2 expression and the upregulation of caspase-3 expression.

Electrophysiological identification of tonic and phasic neurons in sensory dorsal root ganglion and their distinct implications in inflammatory pain.

In the mammalian autonomic nervous system, tonic and phasic neurons can be differentiated on firing patterns in response to long depolarizing current pulse. However, the similar firing patterns in the somatic primary sensory neurons and their functional significance are not well investigated. Here, we identified two types of neurons innervating somatic sensory in rat dorsal root ganglia (DRG). Tonic neurons fire action potentials (APs) in an intensity-dependent manner, whereas phasic neurons typically generate only one AP firing at the onset of stimulation regardless of intensity. Combining retrograde labeling of somatic DRG neurons with fluorescent tracer DiI, we further find that these neurons demonstrate distinct changes under inflammatory pain states induced by complete Freund's adjuvant (CFA) or bee venom toxin melittin. In tonic neurons, CFA and melittin treatments significantly decrease rheobase and AP durations (depolarization and repolarization), enhance amplitudes of overshoot and afterhyperpolarization (AHP), and increase the number of evoked action potentials. In phasic neurons, however, the same inflammation treatments cause fewer changes in these electrophysiological parameters except for the increased overshoot and decreased AP durations. In the present study, we find that tonic neurons are more hyperexcitable than phasic neurons after peripheral noxious inflammatory stimulation. The results indicate the distinct contributions of two types of DRG neurons in inflammatory pain.

A new molecular diagnostic approach to assess Y chromosome microdeletions in infertile men.

OBJECTIVE: A key cause of spermatogenetic failure in infertile males is microdeletions in the azoospermia factor (AZF) regions of the Y chromosome. This study screened for microdeletions in the AZF regions using suspension array technology and compared the results with those from polymerase chain reaction (PCR). METHODS: Patients with spermatogenetic failure (n=507) and healthy control sperm donors (n=100) were recruited. DNA samples were analysed using both multiplex PCR with gel electrophoresis and suspension array technology. RESULTS: The suspension array method identified 45 infertile males with Y chromosome microdeletions, while none was found in the controls. Amongst the AZF subregions, two cases had deletions in AZFa, three in AZFb, 35 in AZFc, three in AZFbc and two in AZFabc. The results from 507 patients were identical when analysed with either suspension array or multiplex PCR, however suspension array technology offered improved sensitivity, may be more accurate and could give time and cost savings. CONCLUSIONS: Suspension array technology offers a rapid and high-throughput method for Y chromosome microdeletion screening in infertile men.

Interferon-ß efficiently inhibited endothelial progenitor cell-induced tumor angiogenesis.

Neovascularization has a critical role in the growth and metastatic spread of tumors, and involves recruitment of circulating endothelial progenitor cells (EPCs) from bone marrow. In this study, we examined whether EPCs could promote tumor angiogenesis, and found that the tumor growth was enhanced by the administration of EPCs. To test the hypothesis that genetically modified bone marrow-derived EPCs can be effective carriers of therapeutic agents to tumor sites, we conducted human interferon-beta (HuIFN-ß) gene transfection of EPCs with a virus vector in vitro. When HuIFN-ß was applied in the ex vivo culture of EPCs, HuIFN-ß-transduced EPCs achieved efficient killing of the total population of SPC-A1 cells, indicating a bystander effect was elicited by HuIFN-ß-transduced EPCs in vitro. When SCP-A1 cancer cells were coimplanted along with ex vivo cultivated EPCs subcutaneous injection in nude mice, the tumor growth was increased. However, the anti-tumor effect of interferon-beta (IFN-ß) offset the tumor-progressive character of EPCs and the tumor growth, and the vascular density of tumor tissues increased by coimplanted EPCs were decreased upon IFN-ß treatment. In addition, overall expression levels of vascular endothelial growth factor in tumor tissues were decreased upon IFN-ß treatment. Therefore, our results suggest that gene-transfected EPCs could be useful as a tumor-specific drug delivery system.

Primary and recurrent embryonal sarcoma of the liver: clinicopathological and immunohistochemical analysis.

AIMS: To evaluate primary and recurrent embryonal sarcoma of the liver and to improve recognition of its morphological variants and immunohistochemical features. METHODS AND RESULTS: Fourteen primary and two recurrent cases of hepatic embryonal sarcoma were evaluated histologically and investigated immunohistochemically with a panel of antibodies using the EnVision+ system. They were usually single, large, globular masses with solid and cystic gelatinous areas. Microscopic features included spindle, oval, stellate, epithelioid or multinucleated cells loosely or densely arranged in a myxomatous matrix. Entrapped bile ducts and hepatic cords were often present at the periphery of the tumours. Intracellular and extracellular periodic acid-Schiff-positive, diastase-resistant hyaline globules were commonly present. Recurrent tumours showed greater cellularity, anaplasia and pluripotential differentiation compared with the primary tumour. Immunohistochemistry showed evidence of widely divergent differentiation into mesenchymal and epithelial phenotypes. CONCLUSIONS: Embryonal sarcoma of the liver may undergo pluripotential differentiation and diagnosis should be based mainly on morphological features. Immunohistochemistry has no specific or diagnostic relevance, but, by using a panel of antibodies, may help to exclude other tumours.