[Efficacy and safety of low-dose rasburicase for refractory chronic gouty arthritis].

Objective: To explore the efficacy and safety of low-dose rasburicase for refractory chronic gouty arthritis. Methods: A cohort study. The clinical data of patients with refractory chronic gouty arthritis who were treated with rasburicase at Sun Yat-sen Memorial Hospital, Sun Yat-sen University between January 2021 and July 2022 were retrospectively analyzed. Refractory chronic gouty arthritis was defined as serum uric acid (sUA)>360 µmol/L and urate volume>10 cm3 under dual-energy computed tomography after tolerable maximal oral urate-lowering therapy for at least 3 months. The administration of low-dose rasburicase was applied intravenously with total dosage ranging from 4.5 to 7.5 mg each dose, at 4-week intervals for a maximum of three doses. Efficacy was evaluated by the changes of sUA level, tophus and urate volume. Results: A total of 22 patients were included for analysis, with 95.4% (21/22) male, the mean age was (44±15) years, and the median duration of gout was 11 (6-15) years. The mean sUA at baseline was (667±112) µmol/L. The levels of sUA significantly decreased after each dose of rasburicase (P<0.001), and the median reduction of sUA after each dose of rasburicase was 568 (471-635), 187 (66-335) and 123 (49-207) µmol/L, respectively. At week 12, nine patients (40.9%) exhibited sUA<360 µmol/L and tophus disappeared in one patient. The urate volume significantly decreased at week 12 when compared with that before the first dose of rasburicase in all the patients [40 (16-172) cm3 vs 17 (7-134) cm3, P<0.001], with a median reduction rate of 41.6% (22.9%-58.5%). The everall safety of rasburicase was good, and no serious adverse reactions occurred. Conclusions: Low-dose rasburicase is well-tolerated and effective for decreasing the urate burden in patients with refractory chronic gouty arthritis. Further prospective randomized controlled trials are needed to validate these findings.

LncRNA PAPAS aggravates the progression of gastric cancer through regulating miRNA-188-5p.

Since this paper presents several inaccuracies and mistakes, the article "LncRNA PAPAS aggravates the progression of gastric cancer through regulating miRNA-188-5p, by X. Shi, X. You, W.-C. Zeng, Y.-J. Deng, H.-L. Hong, O.-X. Huang, M.-F. Wang, published in Eur Rev Med Pharmacol Sci 2019; 23 (24): 10761-10768-DOI: 10.26355/eurrev_201912_19778-PMID: 31858543" has been withdrawn. The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/19778.

LncRNA PAPAS aggravates the progression of gastric cancer through regulating miRNA-188-5p.

OBJECTIVE: To uncover the biological effect of long non-coding RNA (lncRNA) PAPAS on the progression of gastric cancer (GC) by mediating microRNA-188-5p (miRNA-188-5p) level. PATIENTS AND METHODS: The relative level of PAPAS was determined in GC tissues and cell lines by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). The Kaplan-Meier method was introduced to assess the prognostic potential of PAPAS in the overall survival of GC patients. Regulatory effects of PAPAS on proliferative, migratory, and invasive abilities of HGC-27 and AGS cells were detected by cell counting kit-8 (CCK-8), transwell, and wound closure assay, respectively. Subsequently, the binding relation between PAPAS and miRNA-188-5p was verified by the Dual-luciferase reporter gene assay. Correlation between expression levels of PAPAS and miRNA-188-5p in GC tissues was explored. Finally, rescue experiments were conducted to uncover the role of PAPAS/miRNA-188-5p axis in the progression of GC. RESULTS: PAPAS was upregulated in GC tissues and cell lines compared to controls. GC patients expressing a high level of PAPAS suffered worse prognosis relative to those with low level. The silence of PAPAS remarkably attenuated proliferative, migratory, and invasive abilities of HGC-27 cells. Overexpression of PAPAS in AGS cells obtained the opposite trends. MiRNA-188-5p was the direct target of PAPAS, which was negatively regulated by PAPAS. MiRNA-188-5p was able to reverse the regulatory effects of PA-PAS on proliferative, migratory, and invasive abilities of GC cells. CONCLUSIONS: LncRNA PAPAS is upregulated in GC and closely related to lymphatic metastasis, distant metastasis, and poor prognosis of GC patients. PAPAS aggravate the malignant progression of GC by negatively regulating the miRNA-188-5p level.

Knockdown of LINC00461 inhibits cell proliferation and induces apoptosis in gastric cancer by targeting LSD1.

OBJECTIVE: To uncover the function of LINC00461 in regulating cellular behaviors of gastric cancer (GC) via targeting LSD1. PATIENTS AND METHODS: LINC00461 level in GC tissues with different tumor node metastasis (TNM) staging and lymphatic metastasis statues was determined by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). In vitro influences of LINC00461 on proliferative and apoptotic rates were evaluated in AGS and SGC-7901 cells. The interaction between LINC00461 and LSD1 was explored by RNA immunoprecipitation (RIP) assay and qRT-PCR. Finally, the potential role of LSD1 in the proliferative ability of GC cells mediated by LINC00461 was assessed. RESULTS: LINC00461 level was higher in GC tissues relative to matched control ones. It was positively correlated to TNM staging and lymphatic metastasis of GC. Knockdown of LINC00461 markedly attenuated viability and the proliferative ability of AGS and SGC-7901 cells, but induced apoptosis. RIP assay demonstrated the interaction between LINC00461 and LSD1. Moreover, LSD1 could reverse the regulatory effect of LINC00461 on the proliferative ability of GC cells. CONCLUSIONS: LINC00461 is upregulated in GC, which is positively related to TNM staging and lymphatic metastasis. LINC00461 mediates proliferation and apoptosis of GC cells, thereafter aggravating the progression of GC.