Baymccullough7123

Objective Earlier comorbidity measures have been developed or validated using the North American population. This study aims to compare five Charlson or Elixhauser comorbidity indices to predict in-hospital mortality using a large electronic medical record database from Shanxi, China. Methods Using the primary diagnosis code and surgery procedure codes, we identified four hospitalized patient cohorts, hospitalized between 2013 and 2017, in Shanxi, China, as follows congestive heart failure (CHF, n=41,577), chronic renal failure (CRF, n=40,419), diabetes (n=171,355), and percutaneous coronary intervention (PCI, n=39,097). We used logistic regression models and c-statistics to evaluate the in-hospital mortality predictive performance of two multiple comorbidity indicator variables developed by Charlson in 1987 and Elixhauser in 1998 and three single numeric scores by Quan in 2011, van Walraven in 2009, and Moore 2017. Results Elixhauser comorbidity indicator variables had consistently higher c-statistics (0.824, 0.843, 0.904, 0.853) than all other four comorbidity measures, across all four disease cohorts. Moore's comorbidity score outperformed the other two score systems in CHF, CRF, and diabetes cohorts (c-statistics 0.776, 0.832, 0.869), while van Walraven's score outperformed all others among PCI patients (c-statistics 0.827). Conclusion Elixhauser comorbidity indicator variables are recommended, when applied to large Chinese electronic medical record databases, while Moore's score system is appropriate for relatively small databases. © 2020 Cai et al.Background It has been demonstrated that circular RNA (circRNA) plays a crucial role in the occurrence and development of tumors, but the diagnostic and predictive value of most circRNAs in tumor patients remains unclear, especially for multiple myeloma (MM). Methods High-throughput circRNA microarray-based sequencing was used to identify the differentially expressed circRNAs in MM. qRT-PCR was then employed to detect hsa_circRNA_101237 expression levels in the bone marrow tissues from 143 MM patients (65 first-episode treatment-naive patients and 78 patients with recurrent/refractory disease), MM cells and bortezomib-resistant MM cell lines. Whether hsa_circRNA_101237 can be used as a potential biomarker and therapeutic target for MM was investigated. Results The average expressions of hsa_circRNA_101237 in the bone marrow tissues from MM patients (especially those with recurrent/refractory disease), MM cells and bortezomib-resistant MM cell lines were increased significantly (P less then 0.01). hsa_circRNA_101237 was overexpressed in patients positive for 13q14 deletion, 1q21 amplification, P53 deletion, and t(4,14) and t(14,16). hsa_circRNA_101237 was closely related to prognosis of the patients, and its high expression was associated with shorter OS and PFS. In addition, those overexpressing hsa_circRNA_101237 were less responsive to bortezomib treatment. Bioinformatic analysis indicated that hsa_circRNA_101237 interacted with 11 miRNAs and 10 candidate mRNAs. This finding may shed new light on the subsequent studies on the working mechanism and functions. Conclusion It was first reported that hsa_circRNA_101237 was significantly upregulated in MM. Nimodipine chemical structure It was indicated that hsa_circRNA_101237 may be a novel biomarker for MM, and it plays a significant role in the occurrence and development of MM. © 2020 Liu et al.Background There is a growing number of evidence which report the relationship of the dual-specificity phosphatases 14 (DUSP14) with physiological and pathological mechanisms in the human body. However, it is still not known what if any role DUSP14 plays in pancreatic cancer. Materials and Methods The study evaluates the levels of DUSP14 in the pancreatic cancer tissues and cell lines using Western blotting and qRT-PCR to assess the levels of the DUSP14 and epithelial-mesenchymal transition (EMT) biomarkers. After the DUSP14 was blocked, the following assays were performed colony formation, assessments of scratch wound and transwell to examine the effects of DUSP14 on the proliferation, migration and invasion of the pancreatic cancer. Results Results showed that there was a significant increase in the level of DUSP14 expression both in the pancreatic cancer tissues and cell lines. Experimental downregulation of DUSP14 induced the inhibition of the capacity of proliferation, migration and invasion of the pancreatic cancer cells. Western blotting analyses showed changes in the levels of expression of the EMT biomarkers, which helped to determine the function of DUSP14 in EMT. Conclusion In conclusion, we suggest that DUSP14 is a novel molecular target that can be used for the treatment of pancreatic cancer. © 2020 Wei et al.Background Pancreatic cancer (PC) is one of the most well-known malignancies with high mortality, but the underlying mechanism of PC remains unknown. Keratin17 (KRT17) expression has been reported in many malignancies, but its functions in PC are not clear. The aim of our study was to evaluate KRT17 expression and its potential role in PC. Methods The online databases GEPIA and THPA were used to identify KRT17 expression in tissues. Quantitative real-time PCR (qRT-PCR) was used to determine KRT17 expression in cell lines. Ki67 and ROS levels were detected by immunofluorescence assay and a 2',7'-dichlorodihydrofluorescein diacetate (DCFH-DA) probe. KRT17 downregulation was induced by the small interfering RNA (siRNA) technique. Proliferation function was evaluated by colony formation assay and RTCA. Migration and invasion were evaluated by transwell migration assay. A Western blot assay was used to detect protein levels. Results KRT17 was overexpressed in PC tissues compared to that in normal tissues. The results showed that Ki67 and ROS levels were decreased in pancreatic cancer cells after transfection with siKRT17. After KRT17 downregulation in PC cell lines, cell viability functions, including proliferation, migration and invasion, and mTOR/S6K1 phosphorylation levels were attenuated. Conclusion KRT17 knockdown significantly inhibited proliferation, migration and invasion in pancreatic cancer cells. © 2020 Li et al.