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). Ninetyeight 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.

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Infectious diseases continue to pose a major threat to worldwide public health. Infections by Coronavirus Disease 2019 have eased but continue to negatively affect international economic development. The situation of other infectious diseases, such as monkeypox and mosquito-borne diseases, became stable in October. Monitoring epidemic situation of infectious diseases can provide rapid insight into global transmission trends and assist in predicting epidemic situations. Visualizations and analyses summarizing the past few weeks of global data on major infectious diseases are provided.

Infectious diseases are a major threat to global health and the economic stability of societies worldwide. To prevent outbreaks, monitoring the growth trends of infectious diseases appears to be particularly important and necessary. Herein, data from epidemiological websites, such as the World Health Organization and National Health Council are used to illustrate the outbreak trends for infectious diseases worldwide. In the context of the COVID-19 pandemic, a global resurgence in other infectious diseases has been observed, particularly influenza in the United States. Proper surveillance and effective strategies are urgently required to keep emerging infectious diseases under control.

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.