Individualized endoscopic management strategy for impacting jujube pits in the upper gastrointestinal tract: a 3-year single-center experience in northern China.

BACKGROUND: Impaction of jujube pits in the upper gastrointestinal (GI) tract is a special clinical condition in the northern Chinese population. Endoscopic removal is the preferred therapy, but there is no consensus on the management strategies. We reported our individualized endoscopic strategies on the jujube pits impacted in the upper GI tract. METHODS: In this retrospective study, we included 191 patients (male: 57; female: 134) who presented to our hospital with ingestion of jujube pits between January 2015 and December 2017. Demographic information, times of hospital visiting, locations of jujube pits, endoscopic procedures, post-extraction endoscopic characteristics were analyzed. Management strategies including sufficient suction, repeated irrigation, jejunal nutrition and gastrointestinal decompression were given based on post-extraction endoscopic characteristics and impacted locations. RESULTS: Peak incidence was in the second quarter of each year (85/191 cases, 44.5%). Among the 191 cases, 169 (88.5%) showed pits impaction in the esophagus, 20 (10.5%) in the prepyloric region and 2 (1.0%) in the duodenal bulb. A total of 185 patients (96.9%) had pits removed with alligator jaw forceps, and 6 (3.1%) underwent suction removal with transparent caps placed over the end of the endoscope to prevent injury on removal of these pits with two sharp painted edges. Post-extraction endoscopic manifestations included mucosal erosion (26.7%), mucosa laceration (24.6%), ulceration with a white coating (18.9%) and penetrating trauma with pus cavity formation (29.8%). All patients received individualized endoscopic and subsequent management strategies and showed good outcomes. CONCLUSIONS: Individualized endoscopic management for impacted jujube pits in the upper GI tract based on post-extraction endoscopic characteristics and impacted locations was safe, effective, and minimally invasive.

LncRNA-XIST promotes the oxidative stress-induced migration, invasion, and epithelial-to-mesenchymal transition of osteosarcoma cancer cells through miR-153-SNAI1 axis.

Osteosarcoma (OS) is the most common type of primary bone tumor that exhibits invasive growth and long-distance organ metastasis. Thus, investigating the specifically targeted therapeutic agents against metastatic osteosarcoma depends on understanding the molecular mechanisms. The long noncoding RNAs (lncRNA) XIST (X-inactive specific transcript) has been reported to have oncogenic roles in various malignant tumors including OS. However, its molecular mechanisms in OS migration and invasion are still under investigation. In the current study, we demonstrate that XIST is significantly upregulated in 30 pairs of OS tissues compared with their matched adjacent nontumor tissues by the quantitative reverse transcription polymerase chain reaction. Overexpression of XIST significantly induced the invasion, migration, and the epithelial-to-mesenchymal transition (EMT) phenotype. The epithelial marker, E-cadherin was effectively suppressed by XIST overexpression. On the other way, the mesenchymal marker, Fibronectin, Snail, and Vimentin were significantly activated by exogenous XIST overexpression. Furthermore, we observed XIST was upregulated by the oxidative stress-induced EMT. Bioinformatical analysis indicated that miR-153 has multiple biding sites for XIST and miR-153 was inversely suppressed by oxidative stress. XIST was verified to directly downregulate miR-153 via sponging. We identified the mesenchymal marker, SNAI1 was a direct messenger RNA target of miR-153. Importantly, inhibiting XIST successfully blocked the H2 O2 -induced EMT of OS cells. In conclusion, this work demonstrates that lncRNA-XIST promotes the oxidative stress-induced OS cell invasion, migration, and EMT through the miR-153/SNAI1 pathway, presenting lncRNA-XIST as a promising therapeutic target for treating metastatic OS.

LncRNA-SARCC sensitizes osteosarcoma to cisplatin through the miR-143-mediated glycolysis inhibition by targeting Hexokinase 2.

Chemotherapy is one of the primary treatments used against cancer. Cisplatin is a conventional chemotherapy drug used to treat osteosarcoma; however, due to the development of cisplatin resistance, advantageous therapeutic outcomes and prognosis of osteosarcoma remain low. Thus, investigation of the specific targeted therapies to circumvent the anti-chemoresistance of osteosarcoma depends on understanding the molecular mechanisms underlying cisplatin resistance. Tumor cells display an increased utilization of glycolysis rather than oxidative phosphorylation. This phenomenon is called the "Warburg effect," which presents a survival advantage for tumor cells, leading to chemoresistance. To date, the molecular mechanism underlying osteosarcoma cisplatin resistance remains to be fully elucidated. In this study, we reported the significant down-regulation of the long noncoding RNA-Suppressing Androgen Receptor in Renal Cell Carcinoma (lncRNA-SARCC) in the cells of osteosarcoma and in the specimens from osteosarcoma patients. Moreover, we observed a negative correlation between the lncRNA-SARCC and cisplatin resistance in the osteosarcoma tissues. Overexpression of the lncRNA-SARCC sensitizes osteosarcoma cells to cisplatin. From microarray analysis, we screened several miRNAs, which are significantly regulated by the lncRNA-SARCC in osteosarcoma cells, and revealed that lncRNA-SARCC promoted microRNA-43 (miR-143) expression in osteosarcoma. Interestingly, miR-143 showed the same expression pattern with the lncRNA-SARCC in osteosarcoma patient specimens. By establishing a cisplatin-resistant cell line from Sarcoma Osteogenic-2 (Saos-2), we found the cisplatin-resistant cells with down-regulated expressions of the lncRNA-SARCC and miR-143, but with a higher glycolysis rate compared to that in parental cells. We identified the glycolysis key enzyme, Hexokinase 2 (HK2), as a direct target for miR-143 in osteosarcoma. Restoration of the HK2 expression in the lncRNA-SARCC-overexpressing osteosarcoma cells reversed cisplatin resistance, suggesting that lncRNA-SARCC-mediated cisplatin sensitivity may be via glycolysis in the miR-143-inhibited osteosarcoma cells. Finally, results from both in vitro and in vivo xenograft models demonstrated that the lncRNA-SARCC was an effective therapeutic agent for overcoming cisplatin resistance in osteosarcoma. Our findings suggest an essential axis of the lncRNA-SARCC-miR-143-HK2 in regulation of osteosarcoma chemosensitivity, presenting the lncRNA-SARCC as a new therapeutic target against cisplatin-resistant osteosarcoma.

Risks of Postendoscopic Retrograde Cholangiopancreatography Pancreatitis and Hyperamylasemia After Endoscopic Papillary Balloon Dilation: A Retrospective Analysis.

It is currently unclear whether endoscopic papillary balloon dilation (EPBD) is associated with increased severe postendoscopic retrograde cholangiopancreatography pancreatitis (PEP)-related morbidity owing to conflicting reports. This study aimed to investigate whether EPBD increases the risk of PEP and hyperamylasemia. Clinical data of patients with choledocholithiasis, treated at the Second Affiliated Hospital of Harbin Medical University from January 2015 to December 2016 were analyzed. Patients were divided into the EPBD group and endoscopic sphincterotomy (EST)+EPBD group, and their characteristics and PEP and hyperamylasemia incidences were compared. Incidences related to dilated balloon diameter were also analyzed. There were no significant differences in patient characteristics and the incidences of PEP (2.6% vs. 0%; P=0.257) and hyperamylasemia (4.4% vs. 5.6%; P=0.954) between the 2 groups. Results were similar even with different balloon dilatations. EPBD without endoscopic sphincterotomy did not increase the risk of PEP and hyperamylasemia. It is a safe option for choledocholithiasis patients.

Endoscopic muscularis dissection for upper gastrointestinal subepithelial tumors originating from the muscularis propria.

BACKGROUND AND AIMS: Based on our experience with endoscopic submucosal dissection (ESD) and new endoscopic techniques for endoscopic closure of iatrogenic upper gastrointestinal (upper-GI) perforations, we developed methods to remove upper-GI subepithelial tumors (SETs) originating from the muscularis propria by endoscopic muscularis dissection (EMD). The aim of this study is to evaluate the clinical feasibility and safety of EMD. METHODS: 31 patients with upper-GI SETs originating from the muscularis propria were treated by EMD. The EMD differed from ESD in (1) precutting the overlying mucosa above the lesion by using snare or longitudinal incision instead of circumferential incision, (2) dissecting the complete tumors away from submucosal and muscularis propria tissue by electrical dissection combined with blunt dissection, and (3) closing the wound with clips. Perforations occurring during dissection were closed by endoscopic methods. RESULTS: 30 of 31 tumors were resected completely (96.8 %). One esophageal lesion was resected partially because of severe adhesions with surrounding tissue. Mean resected tumor size was 22.1 mm × 15.5 mm, and mean operation time was 76.8 min (range 15-330 min). Histological diagnosis was gastrointestinal stromal tumor (GIST) in 16 lesions [6 esophageal, 3 cardial, 7 gastric; 6 very low risk and 10 low risk according to the National Institutes of Health (NIH) risk classification] and leiomyoma in 15 lesions (8 esophageal, 4 cardial, 3 gastric). No patient developed delayed hemorrhage. Perforation occurred in four patients (12.9 %), all of which were managed successfully by endoscopic techniques. The mean follow-up time was 17.7 months (range 7-35 months). Follow-up found no tumor recurrence in any patient. CONCLUSIONS: In this early experience, EMD appears to be a feasible and minimally invasive treatment for some patients with upper-GI SETs originating from the muscularis propria. Although there is a higher risk of perforation than with ESD, this will improve with extended practice, and perforations have become manageable endoscopically.

Diaqua-bis-[1-ethyl-6-fluoro-4-oxo-7-(piperazin-1-yl)-1,4-dihydroquinoline-3-carboxyl-ato]magnesium(II) hexa-hydrate.

In the title compound, [Mg(C(16)H(17)FN(3)O(3))(2)(H(2)O)(2)]·6H(2)O, the Mg(2+) ion (site symmetry ) exhibits a distorted MgO(6) octa-hedral geometry defined by two O,O-bidentate 1-ethyl-6-fluoro-1,4-dihydro-4-oxo-7-(1-piperazin-yl)-3-quinoline-carb-oxyl-ate (norf) anions and two water mol-ecules. In the crystal, O-H⋯O and O-H⋯N hydrogen bonds help to establish the packing.