[Design and Fabrication of a Device for Intraperitoneal Treatment of Pediatric Hernia].

For treatment of pediatric inguinal hernia, we fabricated a device, i.e. so called "filling type pediatric hernia sac", which treats the problem from the abdominal cavity, through the abdominal and is a self-adaptive closer, using synthetic material. The device includes filling rack, self-adaptive umbrella support bar, bottom piece, outside pulling line and device fixing lines. The filling rack is composed of 2 concentric circles of 3.0 cm diameter with peripherally fixed together and can be pulled into the shapes of a ball or an olive. The supporting bar is structured of 3 pieces with 0.5 cm wide, 4.0 cm long, cross-fixed on top of the filling rack. The bottom piece is in a circular structure with a diameter of 3.0 cm, and it is connected to the filling rack bottom. Adjust positioning stay outside the fixed on the top of the device are connected at one end, and the other end free through filling the top frame connected with the bottom slice of central fixation. By using this device, we treated 37 pediatric inguinal hernia cases with 38 side-inguinal hernia successfully. The mean duration of post-operation follow-ups was 14.6 ± 5.89 months, without hernia recurrence, obvious scar and hard sections of inguinal region. This device could provide a convenient, safe and effective plugging technology for children's pediatric hernia.

Critical role of myeloid differentiation factor 88 in necrotizing enterocolitis.

BACKGROUND: The importance of toll-like receptor 4 in necrotizing enterocolitis (NEC) has been intensively studied, but its downstream signaling and the potential regulatory mechanisms remain unidentified. Our study focused on the role of myeloid differentiation factor 88 (MyD88), the first downstream adaptor of toll-like receptor 4 inflammatory and apoptotic signaling in the pathogenesis of NEC. METHODS: MyD88 knockout (MyD88(-/-)-Ko) mice and lentivirus-mediated stable MyD88-knockdown cell line (IEC-6) were used. NEC was induced by formula gavage, cold, hypoxia, combined with lipopolysaccharide (LPS) in vivo, or LPS stimulation in vitro. NEC was evaluated by histology and multiple inflammatory cytokines. Enterocyte apoptosis was evaluated by terminal-deoxynucleoitidyl transferase-mediated nick end labeling (TUNEL) or Annexin analysis. Inflammatory or apoptotic molecules including NF-κB, Toll/IL-1R domain-containing adaptor-inducing IFN-ß, interferon regulatory factor 3, Bax, Bcl-2, and caspases were examined by quantitative real-time PCR (qRT-PCR). RESULTS: In the MyD88-Ko group, NEC severity and intestinal enterocyte apoptosis rate were reduced, the expression of NF-κB, caspases, and Bax, were all downregulated, while Toll/IL-1R domain-containing adaptor-inducing IFN-ß and were upregulated, and antiapoptotic gene Bcl-2 remained stable. Cytokine levels of interleukin (IL)-6, IL-1ß, and tumor necrosis factor-α (TNF-α) were also all decreased. CONCLUSION: MyD88-dependent signaling is the prevailing inflammatory and apoptotic signaling in toll-like receptor 4 downstream signaling; MyD88-Ko resulted in reduced inflammatory severity and apoptosis, though MyD88-independent signaling can also be activated, but is of less dominant for the development of NEC.

[The set-up of an in vitro model for stable knockdown of MyD88 by lentivirus-based RNAi in IEC-6 cell line and the study on its early apoptosis].

Intestinal inflammatory disease is a kind of non-specific disease with morbidity increasing yearly. It has been proved that the Toll like receptor 4 (TLR4) signaling pathways are closely related to intestinal inflammatory diseases. Myeloid differentiation protein 88 (Myd88) is a critical adaptor protein of TLR4 signaling and critical for the study of intestinal inflammatory disease, but stable Myd88 knockdown in vitro models of cell line are still very few. In the present study, an HIV-1-based lentivirus three-plamid packaging system was used for the construction of a lentivirual vector mediating RNA interference (RNAi) against Myd88 in intestinal fossae epithelial cell line-6 (IEC-6). Real-time PCR and Western blot were used to detect Myd88 expression. Annexin V staining and flowcytometry (FLM) were applied to detect and evaluate the early apoptosis. The results showed that lentiviral vectors containing the shRNA expression cassette specifically targeting Myd88 were constructed and efficiently stably knocked down Myd88 expression in IEC-6 cell line. Early apoptosis was significantly decreased after Myd88 knockdown. This study successfully constructed a lentivirus-based RNAi for Myd88 and detailed the key technique combined with characteristics of the early apoptosis after the Myd88 knockdown, provided a novel, stable and repeatable in vitro model for the pathogenesis, targeting therapeutic study for the intestinal inflammatory diseases.

The Management of Indirect Inguinal Hernia Sac in Laparoscopic Inguinal Hernia Repair: A Systemic Review of Literature.

BACKGROUND: The aim of this study is to investigate the current management strategy of indirect hernia sac during laparoscopic inguinal hernia repair. OBJECTIVES: The aim was to evaluate the various indirect hernia sac management strategies when performing laparoscopic inguinal hernia repair. DATA SOURCES: Major databases (PubMed, Embase, Springer, and Cochrane Library). REVIEW METHODS: MeSH and free-text searching include "laparoscopic inguinal hernia" "TAPP," "TEP," "inguinal hernia," "indirect inguinal hernia sac," "distal sac," "sac transection," "sac ligation," and "sac reduction." RESULTS: The present study enrolled 7 trials, 4 studies compared the results of indirect hernia sac transection and complete sac reduction. The pooled results indicated that indirect hernia sac transection was associated increased seroma formation (odds ratio=2.74, 95% confidence interval: 1.41-4.31), and there was no statistical difference in the incidence of postoperative pain, operative time, hernia recurrence, and time to return to normal activity between the sac transection and sac reduction groups. Two studies reported the application of adjuncts in the management of distal sac during laparoscopic large inguinoscrotal hernia repair. The seroma formation could be reduced by adjuncts of fixing the distal hernia sac to posterior abdominal wall with either suture or tacks. CONCLUSION: Indirect sac transection during laparoscopic indirect inguinal hernia repair is associated with a higher incidence of postoperative seroma. Additional adjuncts to the divided distal hernia sac, including distal sac fixation with either suture or tacks, are effective methods to prevent postoperative seroma.

Wnt inhibitory factor-1 functions as a tumor suppressor through modulating Wnt/ß-catenin signaling in neuroblastoma.

Neuroblastoma is the most common extracranial solid tumor in childhood and is associated with serious morbidity and mortality. The effective treatment of neuroblastoma remains one of the major challenges in pediatric oncology. The Wnt signaling pathway has been shown to play a significant role in the pathogenesis of adult and pediatric tumors. WIF-1 has been identified as an important Wnt antagonist which inhibits Wnt/ß-catenin signaling by directly binding to Wnt proteins. However, the expression and function of WIF-1 in neuroblastoma remains unknown. The present study showed that WIF-1 was downregulated with high level promoter methylation in neuroblastoma cells, and was significantly upregulated after exposure to demethylating agent. This finding suggests that downregulation of WIF-1 was associated with its promoter methylation in neuroblastoma. To further study the potential function of WIF-1 in neuroblastoma, we constructed a plasmid that over-expressed WIF-1 and transfected the plasmid into one neuroblastoma cell line SK-N-SH. We found that restoration of WIF-1 inhibited the growth and proliferation of neuroblastoma cells in vitro. Moreover, Wnt/ß-catenin signaling activity and target genes expression were reduced by WIF-1 restoration. These results provide support that WIF-1 is downregulated and functions as a tumor suppressor by antagonizing Wnt/ß-catenin signaling in neuroblastoma, suggesting a potential role as a therapeutic target in neuroblastoma.

Rare coexistence of metastatic neuroblastoma of liver and solid pseudo papillary tumor of pancreas: case report and literature review.

Neuroblastoma is the second most common malignant solid tumor in children, and often metastasizes to liver, most notably in patients with stage 4S tumors. Solid pseudopapillary tumor of the pancreas (SPT) is a pancreatic borderline tumor with low malignant potential. Coexistence of these two tumors in one patient has never been reported before. Hereby, we present a case of an 8-month-old infant with coexisting tumors of SPT and metastatic neuroblastoma of liver. Dysdifferentiation of neural crest might be responsible for histogenesis of the coexisting tumors.