Endoscopic ultrasound (EUS) and endoscopic resection play an important role in gastric submucosal tumor. However, there were few articles regarding EUS and endoscopic resection of gastric schwannomas. Our aim was to evaluate the role of EUS and endoscopic resection in treating gastric schwannomas.We retrospectively reviewed 14 patients between March 2012 and April 2016 with gastric schwannomas and who received EUS and endoscopic resection. EUS characteristics, endoscopic resection, tumor features, and follow-up were evaluated in all the patients.Fourteen patients were enrolled in the present study. The patients’ ages ranged from 25 to 72 years (mean age, 52.6 years). On EUS, all tumors were originating from muscularis propria and hypoechoic. Ten tumors have the extraluminal growth patterns and 4 tumors have the intraluminal growth patterns. Marginal halos were observed in 7 lesions. No cystic change and calcification were found inside the lesions. Complete endoscopic resection was performed in all the patients with no complications occurring in any patients. No recurrence or metastases was found in all patients during the follow-up period.Gastric schwannoma has some characteristics on EUS, but it is difficult to differentiate gastric schwannoma from gastrointestinal stromal tumor. Endoscopic resection is an effective and safe treatment for gastric schwannoma with an excellent follow-up outcome.
The aim of this study was to investigate the expression of neutrophil gelatinase-associated lipocalin (NGAL) and kidney injury molecule-1 (KIM-1) in the serum, urine and renal tissues of children with acute kidney injury (AKI) and Henoch-Schönlein purpura nephritis (A-on-C). A prospective single-center evaluation of the serum, urine and renal NGAL and KIM-1 levels was performed in a cohort of children. Blood and 5-ml urine samples were collected from each patient for the analysis of NGAL and KIM-1 levels using an ELISA. In addition, the expression of NGAL and KIM-1 in the kidney was examined using immunohistochemistry in patients with A-on-C and HSPN. The expression of serum cystatin C, β2-macroglobulin and serum creatinine (SCr), as well as urinary β2-MG and SCr, in the patients with A-on-C was significantly higher than that of HSPN patients, and the expression of NGAL and KIM-1 in the serum and urine in the A-on-C patients was also significantly higher than that of HSPN patients. However, there were no significant differences in the urine protein levels between the two groups. NGAL and KIM-1 were expressed in renal tubular epithelial cells, and the expression of NGAL and KIM-1 in the A-on-C patients was significantly higher than that in HSPN patients. In addition, the urine NGAL and KIM-1 levels were negatively correlated with glomerular filtration rate, but there was no significant correlation between the urine NGAL/KIM-1 and urine protein levels. The changes in serum and urine NGAL and KIM-1 levels may be applied to the diagnosis of A-on-C.
Objectives:The objective of guideline was to provide clear and relevant consensus statements to form a practical guideline for clinicians on the indications, optimal technique, safety and efficacy of endoscopic ultrasound guided celiac plexus neurolysis (EUS-CPN).Methods:Six important clinical questions were determined regarding EUS-CPN. Following a detailed literature review, 6 statements were proposed attempting to answer those questions. A group of expert endosonographers convened in Chicago, United States (May 2016), where the statements were presented and feedback provided. Subsequently a consensus group of 35 expert endosonographers voted based on their individual level of agreement. A strong recommendation required 80% voter agreement. The modified GRADE (Grading of Recommendations Assessment, Development, and Evaluation) criteria were used to rate the strength of recommendations and the quality of evidence.Results:Eighty percent agreement was reached on 5 of 6 consensus statements, 79.4% agreement was reached on the remaining one.Conclusions:EUS-CPN is efficacious, should be integrated into the management of pancreas cancer pain, and can be considered early at the time of diagnosis of inoperable disease. Techniques may still vary based on operator experience. Serious complications exist, but are rare.
BACKGROUND Pancreatic cancer is a highly malignant tumor of the gastrointestinal system whose emerging resistance to chemotherapy has necessitated the development of novel antitumor treatments. Scoparone, a traditional Chinese medicine monomer with a wide range of pharmacological properties, has attracted considerable attention for its antitumor activity. AIM To explore the potential antitumor effect of scoparone on pancreatic cancer and the possible molecular mechanism of action. METHODS The target genes of scoparone were determined using both the bioinformatics and multiplatform analyses. The effect of scoparone on pancreatic cancer cell proliferation, migration, invasion, cell cycle, and apoptosis was detected in vitro . The expression of hub genes was tested using quantitative reverse transcription polymerase chain reaction (qRT-PCR), and the molecular mechanism was analyzed using Western blot. The in vivo effect of scoparone on pancreatic cancer cell proliferation was detected using a xenograft tumor model in nude mice as well as immunohistochemistry. RESULTS The hub genes involved in the suppression of pancreatic cancer by scoparone were obtained by network bioinformatics analyses using publicly available databases and platforms, including SwissTargetPrediction, STITCH, GeneCards, CTD, STRING, WebGestalt, Cytoscape, and Gepia; AKT1 was confirmed using qRT-PCR to be the hub gene. Cell Counting Kit-8 assay revealed that the viability of Capan-2 and SW1990 cells was significantly reduced by scoparone treatment exhibiting IC 50 values of 225.2 μmol/L and 209.1 μmol/L, respectively. Wound healing and transwell assays showed that scoparone inhibited the migration and invasion of pancreatic cancer cells. Additionally, flow cytometry confirmed that scoparone caused cell cycle arrest and induced apoptosis. Scoparone also increased the expression levels of Bax and cleaved caspase-3, decreased the levels of MMP9 and Bcl-2, and suppressed the phosphorylation of Akt without affecting total PI3K and Akt. Moreover, compared with the control group, xenograft tumors, in the 200 μmol/L scoparone treatment group, were smaller in volume and lighter in weight, and the percentages of Ki65- and PCNA-positive cells were decreased. CONCLUSION Our findings indicate that scoparone inhibits pancreatic cancer cell proliferation in vitro and in vivo , inhibits migration and invasion, and induces cycle arrest and apoptosis in vitro through the PI3K/Akt signaling pathway.
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