Preparation and characterization of fennel (Foeniculum vulgare miller) essential oil/hydroxypropyl-ß-cyclodextrin inclusion complex and its application for chilled pork preservation.

Fennel essential oil (FEO) a natural spice that has versatile biological activities. However, the direct use of FEO is limited due to its water insolubility and poor stability. Chilled pork is prone to spoilage during storage. To solve these problems, this study aimed to prepare an inclusion complex (IC) of FEO with hydroxypropyl-ß-cyclodextrin via co-precipitation and apply it to the preservation of chilled pork. Results indicated that the optimal parameters were encapsulating temperature 37 °C, wall-core ratio 14:1 g/mL, stirring speed 600 r/min, and encapsulating time 240 min, obtaining an encapsulation efficiency of 83.75%. The results of scanning electron microscopy, Fourier transform infra-red spectroscopy, and nuclear magnetic resonance demonstrated the successful preparation of IC. The release of FEO from IC was controllable through adjusting the different temperatures and relative humidities. Furthermore, IC effectively delayed the spoilage of chilled pork and extended its shelf life by 6 days at 4 °C.

Current trends and prospects of surgical techniques for hepatoblastoma.

Hepatoblastoma, a common extracranial malignant solid tumor in childhood, is often detected at an advanced stage and is difficult to treat surgically. Despite the availability of multiple comprehensive treatments that can be combined with surgery, hepatoblastoma treatment outcomes remain poor. Surgery is the main treatment strategy for hepatoblastoma, but it faces many challenges, including tumor attachment to surrounding tissues, tumor wrapping or invading of vital organs and tissues, the presence of giant or multiple tumors, distant metastasis, the formation of a tumor thrombus, and significant surgical trauma. In this review, we discuss recent research advances and propose potential strategies for overcoming these challenges. Such strategies may improve the rate of hepatoblastoma resection and local control in children, as well as reduce complications and trauma.

Robotic resection of paediatric solid tumours at a single institution.

BACKGROUND: To explore the clinical application of robotic-assisted surgery in paediatric solid tumours and to explore its feasibility. METHODS: From 2015 to 2022, 53 children with solid tumours underwent robotic-assisted surgery in our centre were retrospectively analysed. RESULTS: The mean weight of the patients was 27.7 kg, and the mean age was 6.7 years. The average tumour volume was 5.5*4.6*3.7 cm. Two procedures (3.8%) were converted. The mean total operative time was 198.5 min. The mean estimated blood loss was 27.1 ml, and no intraoperative complications occurred. Two (3.8%) patients had postoperative complications. At a median follow-up of 21.2 months, one (1.9%) patient with malignant tumours stopped treatment, and two (3.8%) patients developed tumour recurrence. CONCLUSIONS: Robotic-assisted tumour resection is feasible in highly selected cases of young age, light weight, huge tumour or malignant tumour.

Long noncoding RNA metastasis-associated lung adenocarcinoma transcript 1 cooperates with enhancer of zeste homolog 2 to promote hepatocellular carcinoma development by modulating the microRNA-22/Snail family transcriptional repressor 1 axis.

Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is an oncogenic long noncoding RNA that has been found to promote carcinogenesis and metastasis in many tumors. However, the underlying role of MALAT1 in the progression and metastasis of hepatocellular carcinoma (HCC) remains unclear. In this study, aberrantly elevated levels of MALAT1 were detected in both HCC specimens and cell lines. We found that knockdown of MALAT1 caused retardation in proliferation, migration, and invasion both in vivo and in vitro. Mechanistic investigations showed that Snail family transcriptional repressor 1 (SNAI1) is a direct target of microRNA (miR)-22 and that MALAT1 modulates SNAI1 expression by acting as a competing endogenous RNA for miR-22. Inhibition of miR-22 restored SNAI1 expression suppressed by MALAT1 knockdown. Furthermore, MALAT1 facilitated the enrichment of enhancer of zeste homolog 2 (EZH2) at the promoter region of miR-22 and E-cadherin, which was repressed by MALAT1 knockdown. Cooperating with EZH2, MALAT1 positively regulated SNAI1 by repressing miR-22 and inhibiting E-cadherin expression, playing a vital role in epithelial to mesenchymal transition. In conclusion, our results reveal a mechanism by which MALAT1 promotes HCC progression and provides a potential target for HCC therapy.

Runt-related transcription factor 1 promotes apoptosis and inhibits neuroblastoma progression in vitro and in vivo.

BACKGROUND: Runt-related transcription factor 1 (RUNX1) is a heterodimeric transcription factor that binds to the core element of many enhancers and promoters and can accelerate apoptosis in various tumors. However, the regulatory mechanisms underlying RUNX1 expression in neuroblastoma (NB), a highly malignant tumor in childhood, remain largely unclear. In this study, we aimed to assess the role of RUNX1 in NB and to reveal the underlying mechanisms that may contribute to finding a potential therapeutics strategy against NB. METHODS: Growth, invasion, metastasis and angiogenesis were assessed using Cell Counting Kit-8 (CCK-8) immunocytochemistry, and studies involving soft agar, cell invasion, tube formation and whole animals. The levels of expression were measured using real-time quantitative PCR for RNA, Western blot and immunostaining analyses for proteins. Luciferase reporter and chromatin immunoprecipitation assays indicated that RUNX1 directly binds within the BIRC5, CSF2RB and NFKBIA promoter regions to facilitate transcription. The level of apoptosis was assessed by determining mitochondrial membrane potential and flow cytometry. RESULTS: RUNX1 was highly expressed in ganglioneuroma (GN) and well-differentiated (WD) tissues relative to the poorly differentiated (PD) and undifferentiated (UD) ones. Moreover, RUNX1 effectively reduced cell viability, invasion, metastasis, angiogenesis, and promoted apoptosis in vitro and in vivo. RUNX1 reduced BIRC5 transcription and increased CSF2RB and NFKBIA transcription by directly binding BIRC5, CSF2RB and NFKBIA promoters. In addition, cytotoxic drugs, especially cisplatin, significantly increased RUNX1 expression in NB cells and promoted apoptosis. CONCLUSIONS: These data show that RUNX1 is an independent surrogate marker for the progression of NB and it can be used for monitoring NB prognosis during therapy.

Two-Staged Versus Three-Staged Laparoscopic Anorectoplasty for Patients with Rectoprostatic and Bladder Neck Fistulas: A Comparative Study.

Purpose: To compare the results of two- versus three-staged laparoscopic anorectoplasty (LARP) in children with rectoprostatic and bladder neck fistulas. Materials and Methods: The present study was retrospectively initiated among 32 consecutive patients who underwent two-staged LARP from October 2010 to December 2012. The associated defects, age at the operation, operative time, complications, length of the postoperative hospital stay, total hospitalization cost, and functional results (according to the Krickenbeck scoring system) were evaluated. The results were compared with those of 19 cases who underwent three-staged LARP from October 2008 to September 2010. Results: The average age at the second operation was 4.5 ± 1.2 months in the two-staged group, and 4.2 ± 1.3 months in the three-staged group. In the two-staged group, there were statistically shorter overall operative time and postoperative hospital stay duration. Also, a significantly lower total hospitalization cost was achieved. There was no anastomotic leak in either group. The rates of perineal wound infection, recurrent fistula, and rectal prolapse were 3.85% versus 0% (P = 1.000), 0% versus 5.3% (P = .422), and 11.5% versus 15.8% (P = .686), respectively (two-staged versus three-staged group). The median follow-up time was 67 (range, 54-80) months and 88 (range, 81-104) months, respectively. No significant difference in functional outcome was observed. Conclusions: Two-staged LARP is feasible, safe, and more cost-effective, with comparable incidences of complications and functional outcomes with respect to a three-staged procedure.

EZH2 promotes hepatocellular carcinoma progression through modulating miR-22/galectin-9 axis.

BACKGROUND: Recent studies have shown that interferon-γ (IFN-γ)-induced galectin-9 expression in Kupffer cells plays an essential role in modulatingthe microenvironment of hepatitis-associated hepatocellular carcinoma (HCC). However, whether or not IFN-γ induces galectin-9 expression in HCC cells, its biological role and regulatory mechanism in HCC development and progression are poorly defined. METHODS: Quantitative PCR and western blotting analysis were used to detect galectin-9 and EZH2 levels in HCC cell lines stimulated with IFN-γ. Bioinformatics analysis and luciferase reporter assay were utilized to confirmthe binding ofmiR-22 to the 3' untranslated region (3'-UTR) of galectin-9. The methylation status of miR-22 promoter was analyzed by MSP (Methylation specific PCR) and BSP (bisulfite sequencing PCR), while chromatin immunoprecipitation (ChIP) assay identify the occupation status of EZH2 and H3K27me3 at the promoter. Furthermore, the effect of ectopic expression of galectin-9 and miR-22 on cell proliferation, migration, invasion and cell apoptosis was assessed by using CCK-8, transwell assays and flow cytometric analysis, respectively. RESULTS: IFN-γ induces up-regulation of galectin-9 and EZH2 in HCC cell lines. Galectin-9 is a target of miR-22 and EZH2 facilitates galectin-9 expression by tri-methylation of H3K27 on miR-22 promoter but not hyper-methylation status of DNA. MiR-22 overexpression suppressed HCC cell growth, invasion, and metastasis both in vitro and in vivo. Interestingly, galectin-9 also exhibited antitumor effects, and restoring galectin-9 expression in miR-22 overexpressing cells strengthened its antitumor effects. CONCLUSIONS: These findings indicated that EZH2 facilitates galectin-9 expression by epigenetically repressing miR-22 and that galectin-9, which is known as an immunosuppressant, also functions as a tumor suppressor in HCC.

Neuregulin 1 is involved in enteric nervous system development in zebrafish.

BACKGROUND: Hirschsprung's disease (HD, also known as congenital colon aganglionosis) is a congenital disorder characterized by the absence of intramural ganglion cells in the distal gastrointestinal tract, which results in tonic contraction of the aganglionic gut segment and functional intestinal obstruction. Recent studies have indicated neuregulin 1 (NRG1) as a new candidate gene involved in the development of the enteric nervous system (ENS) in humans. METHODS: In our study, we investigated the role of NRG1 in zebrafish ENS development by assessing NRG1 expression patterns during ENS development. Knockdown, overexpression and rescue zebrafish models of NRG1 were created to evaluate differences in phenotype, numbers of enteric neurons, ENS-related factors and nerve fiber arrangements. RESULTS: NRG1 was expressed in zebrafish intestine at both the larval and adult stage. We also found that decreased expression of NRG1 resulted in reductions in enteric neuron number and decreased expression of ENS development markers. Moreover, NRG1-knockdown zebrafish exhibited a disordered arrangement of nerve fibers. CONCLUSIONS: Collectively, these results demonstrated that NRG1 expression might play a role in zebrafish ENS development. In addition, by modulating NRG1 expression, we created a model that may be useful for investigating the mechanism underlying HD pathogenesis.

Comparison of transumbilical multiport and standard laparoscopic pyeloplasty in children: Mid-term results at a single center.

OBJECTIVE: To compare the efficacy of transumbilical multiport (TMLP) and standard laparoscopic pyeloplasty (SLP) for the treatment of congenital ureteropelvic junction obstruction in children. METHODS: Forty-eight patients were included in this matched-pair study. The TMLP applied three transumbilical incisions for one 5-mm and two 3-mm ports, whereas SLP was undertaken with traditional three-port technique. The demographic, perioperative, and follow-up data were retrospectively compared between TMLP (n=24) and SLP (n=24) groups. RESULTS: Two groups were matched according to patient's age, gender, laterality, weight, and surgical indication. TMLP and SLP were successfully performed in all patients, without conversion to open procedure. There was no significant difference between both groups in intraoperative blood loss, time to oral feeding, time to normal activities, pain scores, or complication rates. Longer mean operative time (125.4±21.6 vs. 112.2±25.2 min; P=0.012) and better patient satisfaction (30.4±4.5 vs. 24.6±3.4; P=0.026) were noted in TMLP group than those in SLP group. Mid-term follow-up indicated no significant difference in postoperative alleviation of hydronephrosis or improvement of renal function. CONCLUSION: TMLP is a feasible and efficient procedure for the management of congenital ureteropelvic junction obstruction in children, with comparative outcome and better cosmetic results than SLP.

microRNA-558 facilitates the expression of hypoxia-inducible factor 2 alpha through binding to 5'-untranslated region in neuroblastoma.

Neuroblastoma (NB) is the most common extracranial solid tumor in childhood. Our previous studies have shown that hypoxia-inducible factor 2 alpha (HIF-2α), one member of the bHLH-PAS transcription factor family, facilitates the progression of NB under non-hypoxic conditions. However, the mechanisms underlying HIF-2α expression in NB still remain largely unknown. Herein, through analyzing the computational algorithm programs, we identified microRNA-558 (miR-558) as a crucial regulator of HIF-2α expression in NB. We demonstrated that miR-558 promoted the expression of HIF-2α at translational levels in NB cells through recruiting Argonaute 2 (AGO2). Mechanistically, miR-558 directly bound with its complementary site within 5'-untranslated region (5'-UTR) to facilitate the binding of AGO2 to eukaryotic translation initiation factor 4E (eIF4E) binding protein 1, resulting in increased eIF4E enrichment and HIF-2α translation. In addition, miR-558 promoted the growth, invasion, metastasis, and angiogenesis of NB cells in vitro and in vivo, and these biological features were rescued by knockdown of AGO2, eIF4E, or HIF-2α. In clinical NB specimens, miR-558, AGO2, and eIF4E were highly expressed and positively correlated with HIF-2α expression. Patients with high miR-558, HIF-2α, AGO2, or eIF4E levels had lower survival probability. Taken together, these results demonstrate that miR-558 facilitates the expression of HIF-2α through bindingto its 5'-UTR, thus promoting the tumorigenesis and aggressiveness of NB.

miRNA-584-5p exerts tumor suppressive functions in human neuroblastoma through repressing transcription of matrix metalloproteinase 14.

Matrix metalloproteinase 14 (MMP-14) is a membrane-anchored MMP crucial for tumorigenesis and aggressiveness, and is highly expressed in neuroblastoma (NB), the most common extracranial solid tumor in childhood. Recent evidence shows the emerging roles of endogenous promoter-targeting microRNAs (miRNAs) in regulating gene transcription. However, the roles of miRNAs in the transcription of MMP-14 still remain largely unknown. In this study, through mining computational algorithm program and Argonaute-chromosome interaction dataset, we identified one binding site of miRNA-584-5p (miR-584-5p) within the MMP-14 promoter. In NB tissues, miR-584-5p was under-expressed and inversely correlated with MMP-14 expression, and was an independent prognostic factor for favorable outcome of patients. miR-584-5p precursor attenuated the expression of MMP-14 in a Dicer-dependent manner, resulting in decreased levels of vascular endothelial growth factor, in cultured NB cell lines. In addition, miR-584-5p suppressed the promoter activity of MMP-14, and mutation of miR-584-5p binding site abolished these effects. Mechanistically, miR-584-5p recruited Argonaute 2 to facilitate the enrichment of enhancer of zeste homolog 2, histone H3 lysine 27 trimethylation, and histone H3 lysine 9 dimethylation on MMP-14 promoter in NB cells, which was abolished by repressing the miR-584-5p-promoter interaction. Gain- and loss-of-function studies demonstrated that miR-584-5p suppressed the growth, invasion, metastasis, and angiogenesis of NB cells in vitro and in vivo. Moreover, restoration of MMP-14 expression rescued the NB cells from changes in these biological features. Taken together, these results indicate that promoter-targeting miR-584-5p exerts tumor suppressive functions in NB through repressing the transcription of MMP-14.

A Modified Approach for Inguinal Hernias in Children: Hybrid Single-Incision Laparoscopic Intraperitoneal Ligation.

PURPOSE: To report a laparoscopic approach for pediatric inguinal hernia repair using a hybrid single-incision laparoscopic (H-SIL) technique and its clinical outcomes. MATERIALS AND METHODS: A retrospective study was carried out in inguinal hernia cases treated with the new H-SIL approach using intracorporeal jumping purse-string sutures. The operative time, length of postoperative hospital stay, efficiency of the operation, and complications were analyzed. RESULTS: In total, 157 inguinal high ligations were performed in 106 children (89 boys, 17 girls). The median age was 1.5 years (range, 25 days-11.6 years). The mean operative time was 15.8±3.4 minutes for the single-side procedure and 20.3±2.5 minutes for bilateral procedures. The mean postoperative hospital stay was 0.99±0.52 (range, 0.25-3 days). No postoperative bleeding, abdominal wall emphysema, abdominal viscera injury, or scrotal edema was found, and there were no known cases of postoperative testicular atrophy or hypotrophy. Ninety-three percent of the patients became fully mobile on the first postsurgical day. The median follow-up period was 17 months (range, 9-21 months), with no recurrence, no visible scars on the abdominal wall, and no foreign body felt in the inguinal region. CONCLUSIONS: This H-SIL approach is a safe and efficient method for pediatric inguinal hernia repair. The maneuverability is the same as that in the triport laparoscopic technique, and the cosmetic results are similar to those of single-port laparoscopic surgery.

miRNA-337-3p suppresses neuroblastoma progression by repressing the transcription of matrix metalloproteinase 14.

Recent evidence shows the emerging roles of endogenous microRNAs (miRNAs) in repressing gene transcription. However, the miRNAs inhibiting the transcription of matrix metalloproteinase 14 (MMP-14), a membrane-anchored MMP crucial for the tumorigenesis and aggressiveness, still remain largely unknown. In this study, through mining computational algorithm program and genome-wide Argonaute profiling dataset, we identified one binding site of miRNA-337-3p (miR-337-3p) within the MMP-14 promoter. We demonstrated that miR-337-3p was under-expressed and inversely correlated with MMP-14 expression in clinical specimens and cell lines of neuroblastoma (NB), the most common extracranial solid tumor in childhood. Patients with high miR-337-3p expression had greater survival probability. miR-337-3p suppressed the promoter activity, nascent transcription, and expression of MMP-14, resulting in decreased levels of vascular endothelial growth factor, in cultured NB cell lines. Mechanistically, miR-337-3p recognized its binding site and recruited Argonaute 2 to facilitate the enrichment of repressive epigenetic markers and decrease the binding of RNA polymerase II and specificity protein 1 on the MMP-14 promoter. Gain- and loss-of-function studies demonstrated that miR-337-3p suppressed the growth, invasion, metastasis, and angiogenesis of NB cells in vitro and in vivo. In addition, restoration of MMP-14 expression rescued the NB cells from changes in these biological features. Taken together, these data indicate that miR-337-3p directly binds the MMP-14 promoter to repress its transcription, thus suppressing the progression of NB.

Intelectin 1 suppresses tumor progression and is associated with improved survival in gastric cancer.

Recent evidence shows the emerging roles of intelectin 1 (ITLN1), a secretory lectin, in human cancers. Our previous studies have implicated the potential roles of ITLN1 in the aggressiveness of gastric cancer. Herein, we investigated the functions, downstream targets, and clinical significance of ITLN1 in the progression of gastric cancer. We demonstrated that ITLN1 increased the levels of hepatocyte nuclear factor 4 alpha (HNF4α), resulting in suppression of nuclear translocation and transcriptional activity of ß-catenin in gastric cancer cells. Mechanistically, ITLN1 attenuated the activity of nuclear factor-kappa B, a transcription factor repressing the HNF4α expression, in gastric cancer cells through inactivating the phosphoinositide 3-kinase/AKT/Ikappa B kinase signaling. Gain- and loss-of-function studies demonstrated that ITLN1 suppressed the growth, invasion, and metastasis of gastric cancer cells in vitro and in vivo. In addition, restoration of HNF4α expression prevented the gastric cancer cells from ITLN1-mediated changes in these biological features. In clinical gastric cancer tissues, HNF4α expression was positively correlated with that of ITLN1. Patients with high ITLN1 or HNF4α expression had greater survival probability. Taken together, these data indicate that ITLN1 suppresses the progression of gastric cancer through up-regulation of HNF4α, and is associated with improved survival in patients with gastric cancer.

Intelectin 1 suppresses the growth, invasion and metastasis of neuroblastoma cells through up-regulation of N-myc downstream regulated gene 2.

BACKGROUND: Recent studies have revealed the potential roles of intelectin 1 (ITLN1) in tumorigenesis. However, its functions and underlying mechanisms in neuroblastoma (NB), the most common extracranial solid tumor in childhood, still remain largely unknown. METHODS: Human neuroblastoma cell lines were treated with recombinant ITLN1 protein or stably transfected with ITLN1 expression and short hairpin RNA vectors. Gene expression and signaling pathway were detected by western blot and real-time quantitative RT-PCR. Gene promoter activity and transcription factor binding were detected by luciferase reporter and chromatin immunoprecipitation assays. Growth and aggressiveness of tumor cells were measured by MTT colorimetry, colony formation, scratch assay, matrigel invasion assay, and nude mice model. RESULTS: Mining of public microarray databases revealed that N-myc downstream regulated gene 2 (NDRG2) was significantly correlated with ITLN1 in NB. Gain- and loss-of-function studies indicated that secretory ITLN1 facilitated the NDRG2 expression, resulting in down-regulation of vascular endothelial growth factor (VEGF) and matrix metalloproteinase 9 (MMP-9), in NB cell lines SH-SY5Y, SK-N-BE(2), and SK-N-SH. Krüppel-like factor 4 (KLF4), a transcription factor crucial for NDRG2 expression, was up-regulated by ITLN1 in NB cells via inactivation of phosphoinositide 3-kinase (PI3K)/AKT signaling. Ectopic expression of ITLN1 suppressed the growth, invasion and metastasis of NB cells in vitro and in vivo. Conversely, knockdown of ITLN1 promoted the growth, invasion, and metastasis of NB cells. In addition, rescue experiments in ITLN1 over-expressed or silenced NB cells showed that restoration of NDRG2 expression prevented the tumor cells from ITLN1-mediated changes in these biological features. In clinical NB tissues, ITLN1 was down-regulated and positively correlated with NDRG2 expression. Patients with high ITLN1 or NDRG2 expression had greater survival probability. CONCLUSIONS: These findings indicate that ITLN1 functions as a tumor suppressor that affects the growth, invasion and metastasis of NB through up-regulation of NDRG2.

Hepatocyte nuclear factor 4 alpha promotes the invasion, metastasis and angiogenesis of neuroblastoma cells via targeting matrix metalloproteinase 14.

Matrix metalloproteinase 14 (MMP-14) is the only membrane-anchored MMP that plays critical roles in tumorigenesis and aggressiveness. However, the regulatory mechanisms underlying the high MMP-14 expression in neuroblastoma (NB), a highly malignant tumor in childhood, still remain unclear. Herein, we applied an integrative approach to analyze the public datasets, and identified hepatocyte nuclear factor 4 alpha (HNF4α) as a crucial transcription factor facilitating the MMP-14 expression in NB. In clinical NB tissues, HNF4α was up-regulated and positively correlated with MMP-14 expression, and was an independent prognostic factor for unfavorable outcome of patients. Luciferase reporter and chromatin immunoprecipitation assays indicated that HNF4α directly targeted the binding site within the MMP-14 promoter to facilitate its transcription. Knockdown of HNF4α suppressed the invasion, metastasis and angiogenesis of NB cells in vitro and in vivo. Conversely, ectopic expression of HNF4α promoted the invasion, metastasis and angiogenesis of NB cells. Importantly, restoration of MMP-14 expression prevented the tumor cells from HNF4α-mediated changes in these biological features. Taken together, HNF4α exhibits oncogenic activity that affects the aggressiveness and angiogenesis of NB through activating the transcription of MMP-14.

miRNA-558 promotes tumorigenesis and aggressiveness of neuroblastoma cells through activating the transcription of heparanase.

Heparanase (HPSE) is the endogenous endoglycosidase that degrades heparan sulfate proteoglycans and promotes the tumor growth, invasion, metastasis and angiogenesis. Our previous studies have shown that HPSE is highly expressed in neuroblastoma (NB), the most common extracranial solid tumor in childhood. However, the underlying regulatory mechanisms remain largely unknown. In this study, we identified one binding site of microRNA-558 (miR-558) within the HPSE promoter. In NB tissues and cell lines, miR-558 was up-regulated and positively correlated with HPSE expression. Gain- and loss-of-function studies demonstrated that miR-558 facilitated the transcript and protein levels of HPSE and its downstream gene, vascular endothelial growth factor, in NB cell lines. In addition, miR-558 enhanced the promoter activities of HPSE, and these effects were abolished by the mutation of the miR-558-binding site. Mechanistically, miR-558 induced the enrichment of the active epigenetic marker and RNA polymerase II on the HPSE promoter in NB cells in an Argonaute 1-dependent manner, which was abolished by repressing the miR-558-promoter interaction. Knockdown of endogenous miR-558 decreased the growth, invasion, metastasis and angiogenesis of NB cells in vitro and in vivo. In contrast, over-expression of miR-558 promoted the growth, invasion, metastasis and angiogenesis of SH-SY5Y and SK-N-SH cells. Restoration of HPSE expression prevented the NB cells from changes in these biological features induced by knockdown or over-expression of miR-558. These data indicate that miR-558 induces the transcriptional activation of HPSE via the binding site within promoter, thus facilitating the tumorigenesis and aggressiveness of NB.

Over-expression of testis-specific expressed gene 1 attenuates the proliferation and induces apoptosis of GC-1spg cells.

The effects of over-expression of testis-specific expressed gene 1 (TSEG-1) on the viability and apoptosis of cultured spermatogonial GC-1spg cells were investigated, and the immortal spermatogonial cell line GC-1spg (CRL-2053™) was obtained as the cell model in order to explore the function of TSEG-1. We transfected the eukaryotic vector of TSEG-1, named as pEGFP-TSEG-1 into cultured spermatogonial GC-1spg cells. Over-expression of TSEG-1 inhibited the proliferation of GC-1spg cells, and arrested cell cycle slightly at G0/G1 phase. Transfection of TSEG-1 attenuated the transcript levels of Ki-67, PCNA and cyclin D1. In addition, over-expression of TSEG-1 induced early and late apoptosis, and reduced the mitochondrial membrane potential of GC-1spg cells. Moreover, transfection of TSEG-1 significantly enhanced the ratio of Bax/Bcl-2 and transcript levels of caspase 9, and decreased the expression of Fas and caspase 8 in GC-1spg cells. These results indicated over-expression of TSEG-1 suppresses the proliferation and induces the apoptosis of GC-1spg cells, which establishes a basis for further study on the function of TSEG-1.

Association of Ureaplasma urealyticum colonization with development of bronchopulmonary dysplasia: a systemic review and meta-analysis.

There is controversy regarding the roles of Ureaplasma urealyticum (U. urealyticum) colonization in the development of bronchopulmonary dysplasia (BPD). This study explored the association between U. urealyticum and bronchopulmonary dysplasia at 36 weeks post-menstrual age (BPD36). Studies published before December 31, 2013 were searched from Medline, Embase, Ovid, Web of Science, and Cochrane databases, with the terms "Ureaplasma urealyticum", "chronic lung disease", or "BPD36" used, and English language as a limit. The association between U. urealyticum colonization and BPD36 was analyzed with RevMan 4.2.10 software, using the odds ratio (OR) and relative risk (RR) for dichotomous variables. Out of the enrolled 81 studies, 11 investigated the BPD36 in total 1193 infants. Pooled studies showed no association between U. urealyticum colonization and subsequent development of BPD36, with the OR and RR being 1.03 (95% CI=0.78-1.37; P=0.84) and 1.01 (95% CI= 0.88-1.16, P=0.84), respectively. These findings indicated no association between U. urealyticum colonization and the development of BPD36.

Nuss repair of pectus excavatum after surgery for congenital heart disease: experience from a single institution.

OBJECTIVE: Pectus excavatum developing after surgery for congenital heart disease has its own clinical characteristics. The present study aimed to present our technique and outcomes for the Nuss procedure in the repair of these cases. METHODS: We conducted a retrospective study of all patients who had not been diagnosed as pectus excavatum preoperatively but subsequently had developed pectus excavatum after surgery for congenital heart disease from February 2005 to November 2012. The Nuss procedure was applied using a series of perioperative management techniques. The data relating to the surgical technique, complications, and outcomes were analyzed. The clinical evaluation was performed using the Nuss criteria. RESULTS: A total of 30 cases (14 boys and 16 girls) were included. The mean operative time was 73.5 minutes (range, 58-82). The mean length of hospital stay was 6.0 days. Complications occurred in 5 patients (16.7%), including asymptomatic pneumothorax, hematoma in the wound, pericardial penetration, and bar displacement. The mean follow-up period was 32 months (range, 9-60). Initially, 29 patients (96.7%) had excellent results, and 1 patient had a good result. The mean point of bar removal was 35.8 months (range, 30-39) after implantation. The postoperative results after bar removal in 17 patients were also recorded, including excellent results in 14 (82.4%), good results in 2 (11.7%), and a fair result in 1 patient. CONCLUSIONS: The Nuss procedure has been shown to be a safe and effective approach for the repair of pectus excavatum after surgery for congenital heart disease, although dissection of substernal adhesions can increase the risk of heart injury.