The Value of RANSON Score Combined with BMI in Predicting the Mortality in Severe Acute Pancreatitis: A Retrospective Study.

Objective: To explore the value of modified RANSON score in predicting mortality from severe acute pancreatitis (SAP). Methods: In this retrospective study, 461 SAP patients hospitalized from January 2016 to January 2020 were enrolled. AP (acute pancreatitis) patients from our hospital were employed as the training set. In addition, AP patients from the affiliated hospital of Nantong University were set as the validation set. The clinical characteristics of patients were compared between the two sets. The independent risk factors for SAP were determined through logistic regression. Moreover, the risk factors were derived for various prediction models by logistic regression. Multiple methods were adopted to assess the predictive ability of various models. Results: A total of 338 patients were assigned into the training set, while 123 patients were assigned into the validation set. The patients in the training and validation sets showed the consistent distribution trends (P>0.05). In the training set, significant differences between patients in the non-survival and survival groups were BMI, PCT, platelets (PLT), direct bilirubin (DBil) and RANSON scores (P<0.05). In further multivariate analysis, BMI, PCT and RANSON score were found as the independent risk factors for the mortality of SAP (OR=1.12, 1.25, 1.28, 95% CI:1.06-1.19, 1.08-1.44, 1.12-1.47, P<0.05). In the training set and validation set, ROC curve analysis showed that AUC of BMI+RANSON score was 0.778 and 0.789, respectively. In the calibration curve, the fitting degree of RANSON score+BMI and ideal assessment model was 0.975 and 0.854, respectively. The decision curve suggested that the net benefit per patient increased with the lengthening of the RANSON score+ BMI model curve. As revealed by the results of NRI and IDI indicators, RANSON score+BMI was optimized based on RANSON score (P<0.05). Conclusion: BMI+RANSON was confirmed as a modified model effective in predicting the mortality from SAP.

A comprehensive expression profile of tRNA-derived fragments in papillary thyroid cancer.

BACKGROUND: The incidence of thyroid cancer has been on a rise. Papillary thyroid cancer (PTC) is the most common type of malignant thyroid tumor and accounts for approximately 85% of thyroid cancer cases. Although the genetic background of PTC has been studied extensively, relatively little is known about the role of small noncoding RNAs (sncRNAs) in PTC. tRNA-derived fragments (tRFs) represent a newly discovered class of sncRNAs that exist in many species and play key roles in various biological processes. METHODS: In this study, we used high-throughput next-generation sequencing technology to analyze the expression of tRFs in samples from PTC tissues and normal tissues. We selected four tRFs to perform qPCR to determine the expression levels of these molecules and make bioinformatic predictions. RESULTS: We identified 53 unique tRFs and transfer RNA halves (tsRNAs). The 10 most upregulated tRFs and tsRNAs were tRF-39-I6D3887S1RMH5MI2, tRF-21-2E489B3RB, tRF-18-JMRPFQDY, tRF-17-202L2YF, tRF-17-VBY9PYJ, tRF-18-YRRHQFD2, tRF-21-WE884U1DD, tRF-41-EX2Z10I9BZBZOS4YB, tRF-39-HPDEXK7S1RNS9MI2, and tRF-20-1SS2P46I. The 10 most downregulated tRFs and tsRNAs were tRF-31-HQ9M739P8WQ0B, tRF-43-5YXENDBP1IUUK7VZV, tRF-38-RZYQHQ9M739P8WD8, tRF-25-9M739P8WQ0, tRF-33-V6Z3M8ZLSSXUD6, tRF-27-MY73H3RXPLM, tRF-26-DBNIB9I1KQ0, tRF-38-Z9HMI8W47W1R7HX, tRF-40-Z6V6Z3M8ZLSSXUOL, and tRF-39-YQHQ9M739P8WQ0EB. qPCR verification of cell lines and tissue samples yielded results consistent with the sequencing analysis. As tRF-39 expression showed the maximum difference between PTC cells and normal cells, we chose this tRF to predict targets and perform functional tRF and tsRNA enrichment analysis. CONCLUSION: In this study, we provided a comprehensive catalog of tRFs involved in PTC and assessed the abnormal expression of these fragments. Through qPCR verification, tRF-39-0VL8K87SIRMM12E2 was found to be the most significantly upregulated tRF. Further tRF and enrichment analysis revealed that tRF-39 was mostly enriched in the "metabolic pathways." These preliminary findings can be used as the basis for further research studies based on the functional role of tRFs in patients with PTC.

MicroRNA-27a-3p Reverses Adriamycin Resistance by Targeting BTG2 and Activating PI3K/Akt Pathway in Breast Cancer Cells.

AIM: This study aimed to explore the regulative mechanisms of miR-27a-3p in chemo-resistance of breast cancer cells. MATERIALS AND METHODS: qRT-PCR was employed to determine miR-27a-3p expression in two breast cancer cell lines, MCF-7 and MCF-7/adriamycin-resistant cell line (MCF-7/ADR). The two cell lines were treated with miR-27a-3p mimics or inhibitors or corresponding negative control (NC), respectively. The changes were investigated by qRT-PCR, CCK-8 assay, Western blot (WB), colony formation assay, and flow cytometry assay. Moreover, luciferase reporter assay was analyzed to verify the downstream target gene of miR-27a-3p. Further investigation in the correlation between miR-27a-3p and BTG2 was launched by WB, flow cytometry assay, and CCK-8 assay. The expression of Akt and p-Akt was detected by WB. KEY FINDINGS: Significantly higher miR-27a-3p expression was confirmed in MCF-7/ADR as compared with sensitive cell line MCF-7 (P<0.05). The down-regulation of miR-27a-3p in MCF-7/ADR enhanced the sensitivity of cancer cells to adriamycin treatment, decreased multidrug resistance gene 1/P-glycoprotein (MDR1/P-gp) expression, enhanced the apoptosis-related proteins expression, increased adriamycin-induced apoptosis, and inhibited cell proliferation as compared to NC groups (P<0.05). The up-regulation of miR-27a-3p in MCF-7 showed the opposite results. BTG2 is identified as a direct target of miR-27a-3p and its down-regulation reversed ADR-resistance. BTG2 treatment exhibited inhibitory effect on PI3K/Akt pathway in MCF-7/ADR cells. SIGNIFICANCE: miR-27a-3p might be associated with resistance of breast cancer cells to adriamycin treatments, modulating cell proliferation and apoptosis by targeting BTG2 and promoting the PI3K/Akt pathway in breast cancer cells. miR-27a-3p/BTG2 axis might be a potential therapeutic target for clinical BC resistance.

Insight into the effects of microRNA-23a-3p on pancreatic cancer and its underlying molecular mechanism.

Previous studies have demonstrated that microRNA (miR)-23a-3p plays a role as an oncogene that is involved in several different types of carcinoma. However, few studies investigated the association between miR-23a-3p and pancreatic cancer (PC). The aim of the present study was to elucidate the biological functions of miR-23a-3p in PC and to investigate its underlying molecular mechanisms. The expression of miR-23a-3p in PC and adjacent normal tissues was investigated using microarrays. In order to validate the outcomes of the microarray results, reverse transcription-quantitative (RT-q)PCR was used to determine the expression levels of miR-23a-3p in PC tissues and cell lines. Furthermore, functional analyses were conducted following miR-23a-3p inhibition and overexpression, in order to assess the proliferation, invasion and migration of PC cells. Bioinformatics analysis indicated transforming growth factor-ß receptor type II (TGFBR2) as a potential direct target of miR-23a-3p. Western blotting was performed in order to determine the protein expression of TGFBR2 in PC cell lines. The findings from the microarray demonstrated upregulation of miR-23a-3p in PC compared with normal tissues. RT-qPCR revealed significantly higher levels of miR-23a-3p expression in PC compared with normal control tissues or cells. Furthermore, miR-23a-3p was demonstrated to promote the proliferation, invasion and migration of PC cells, which was suppressed by the inhibition of miR-23a-3p. In addition, the miR-23a-3p expression level was negatively associated with TGFBR2 expression. Overall, the present study demonstrated the tumor-promoting effects of miR-23a-3p in PC cells. Furthermore, miR-23a-3p is a potential oncogenic regulator of PC, by targeting TGFBR2, and a biomarker or target for molecular therapy.