Analysis of fungal bloodstream infection in intensive care units in the Meizhou region of China: species distribution and resistance and the risk factors for patient mortality.

BACKGROUND: Fungal bloodstream infections (FBI) among intensive care unit (ICU) patients are increasing. Our objective was to characterize the fungal pathogens that cause bloodstream infections and determine the epidemiology and risk factors for patient mortality among ICU patients in Meizhou, China. METHODS: Eighty-one ICU patients with FBI during their stays were included in the study conducted from January 2008 to December 2017. Blood cultures were performed and the antimicrobial susceptibility profiles of the resulting isolates were determined. Logistic multiple regression and ROC curve analysis were used to assess the risk factors for mortality among the cases. RESULTS: The prevalence of FBI in ICU patients was 0.38% (81/21,098) with a mortality rate of 36% (29/81). Ninety-eight strains of bloodstream-infecting fungi, mainly Candida spp., were identified from these patients. Candida albicans was most common (43%). Two strains of C. parapsilosis were no-sensitive to caspofungin, C. glabrata were less than 80% sensitive to azole drugs. Logistic multiple regression showed that age, serum albumin, APACHE II score, three or more underlying diseases, and length of stay in ICU were independent risk factors for mortality in FBI. ROC curve analysis showed that APACHE II scores > 19 and serum albumin ≤25 g/L were the best predictors of mortality. CONCLUSION: Candida spp. predominated with high mortality rates among cases of FBI in ICU. Thus, clinical staff should enhance overall patient monitoring and concurrently monitor fungal susceptibility to reduce mortality rates.

Long non-coding RNA BC002811 Promotes Gastric Cancer Metastasis by Regulating SOX2 Binding to the PTEN Promoter.

There is increasing evidence that long non-coding RNAs (lncRNAs) are involved in the pathogenesis and progression of gastric cancer (GC), however, the underlying mechanisms remain poorly understood. In this study, we identified lncRNA BC002811 as a critical regulator of GC development and progression. BC002811 was upregulated in GC tissues and cell lines, and that high expression of BC002811 was indicative of a reduction in overall survival of GC patients. Our research reveals that BC002811 promoted GC cell proliferation, migration, invasion, and inhibition of apoptosis in vitro, as well as accelerated tumor growth and metastasis in vivo. We also found that BC002811 upregulated MMP2 and MMP9 and promoted GC cell metastasis partially through downregulating PTEN expression. BC002811 may act as a molecular decoy for the transcription factor SOX2, thereby inhibiting the transcription of PTEN by blocking SOX2 binding to the PTEN promoter. Our study advances the understanding of the role of BC002811 in the pathogenesis of GC and provides new molecular targets for therapeutic intervention against GC metastasis.

Differential gene expression analysis after DAPK1 knockout in hepatocellular carcinoma cells.

Background: The mechanism through which death-associated protein kinase 1 (DAPK1) causes hepatocellular carcinoma (HCC) progression remains unclear. In this study, we aimed to identify key proteins that were altered after DAPK1 knockout. Methods: Stable DAPK1 knockout HCC cell lines were established, then the differentially expressed genes (DEGs) of HCC were screened using the NetworkAnalyst database and enriched using the Metascape software. Protein-protein interaction networks (PPIs) were analyzed and visualized using the STRING database expansion. Results: In total, 732 differentially expressed genes were identified, including 415 upregulated genes and 317 downregulated genes. Through Cytoscape software scoring, 10 pivotal genes were found to be closely related to changes in DAPK1 expression; Kininogen-1 (KNG1), Complement C3 (C3), Metalloproteinase inhibitor 1 (TIMP1), and Alpha-2-HS-glycoprotein (AHSG) were the most strongly associated with DAPK1 expression changes. Moreover, western blot analysis results revealed that changes in the levels of proteins encoded by the four key genes after DAPK1 knockout were consistent with those seen in the database screening. Conclusions: These results provide a direction for further studies on the DAPK1 gene and on the mechanism through which DAPK1 leads to hepatocellular carcinoma development.