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Purpose: Predicting future outbreaks and understanding how they are spreading from location to location can improve patient care provided. Recently, mining social media big data provided the ability to track patterns and trends across the world. This study aims to analyze social media micro-blogs and geographical locations to understand how disease outbreaks spread over geographies and to enhance forecasting of future disease outbreaks. Design/methodology/approach: In this paper, the authors use Twitter data as the social media data source, influenza-like illnesses (ILI) as disease epidemic and states in the USA as geographical locations. They present a novel network-based model to make predictions about the spread of diseases a week in advance utilizing social media big data. Findings: The authors showed that flu-related tweets align well with ILI data from the Centers for Disease Control and Prevention (CDC) (p< 0.049). The authors compared this model to earlier approaches that utilized airline traffic, and showed that ILI activity estimates of their model were more accurate. They also found that their disease diffusion model yielded accurate predictions for upcoming ILI activity (p< 0.04), and they predicted the diffusion of flu across states based on geographical surroundings at 76 per cent accuracy. The equations and procedures can be translated to apply to any social media data, other contagious diseases and geographies to mine large data sets. Originality/value: First, while extensive work has been presented utilizing time-series analysis on single geographies, or post-analysis of highly contagious diseases, no previous work has provided a generalized solution to identify how contagious diseases diffuse across geographies, such as states in the USA. Secondly, due to nature of the social media data, various statistical models have been extensively used to address these problems.

Nonalcoholic fatty liver disease (NAFLD) is associated with an increased risk of cardiovascular disease. Because the liver is the major source of circulatory proteins, it is not surprising that hepatic disease could lead to alterations in the plasma proteome, which are therein implicated in atherosclerosis. The current study used low-density lipoprotein receptor-deficient (LDLR–/–) mice to examine the impact of Western diet (WD)-induced NAFLD on plasma proteome homeostasis. Using a 2H2O-metabolic labeling method, we found that a WD led to a proinflammatory distribution of circulatory proteins analyzed in apoB-depleted plasma, which was attributed to an increased production. The fractional turnover rates of short-lived proteins that are implicated in stress-response, lipid metabolism, and transport functions were significantly increased with WD (P< 0.05). Pathway analyses revealed that alterations in plasma proteome dynamics were related to the suppression of hepatic PPARα, which was confirmed based on reduced gene and protein expression of PPARα in mice fed a WD. These changes were associated with ∼4-fold increase (P< 0.0001) in the proinflammatory property of apoB-depleted plasma. In conclusion, the proteome dynamics method reveals proinflammatory remodeling of the plasma proteome relevant to liver disease. The approach used herein may provide a useful metric of in vivo liver function and better enable studies of novel therapies surrounding NAFLD and other diseases.

Piwi proteins are a subfamily of Argonaute proteins that maintain germ cells in eukaryotes. However, the role of their human homologs in cancer stem cells, and more broadly in cancer, is poorly understood. Here, we report that Piwi-like family members are overexpressed in glioblastoma (GBM), with Piwil1 (Hiwi) most frequently overexpressed (88%). Piwil1 is enriched in glioma stem-like cells (GSCs) to maintain self-renewal. Silencing Piwil1 in GSCs leads to global changes in gene expression resulting in cell-cycle arrest, senescence, or apoptosis. Piwil1 knockdown increases expression of the transcriptional co-regulator BTG2 and the E3-ubiquitin ligase FBXW7, leading to reduced c-Myc expression, as well as loss of expression of stem cell factors Olig2 and Nestin. Piwil1 regulates mRNA stability of BTG2, FBXW7, and CDKN1B. In animal models of GBM, Piwil1 knockdown suppresses tumor growth and promotes mouse survival. These findings support a role of Piwil1 in GSC maintenance and glioblastoma progression.

Tumor hypoxia is associated with poor patient survival and is a characteristic of glioblastoma. Notch signaling is implicated in maintaining glioma stem-like cells (GSCs) within the hypoxic niche, although the molecular mechanisms linking hypoxia to Notch activation have not been clearly delineated. Here we show that Vasorin is a critical link between hypoxia and Notch signaling in GSCs. Vasorin is preferentially induced in GSCs by a HIF1α/STAT3 co-activator complex and stabilizes Notch1 protein at the cell membrane. This interaction prevents Numb from binding Notch1, rescuing it from Numb-mediated lysosomal degradation. Thus, Vasorin acts as a switch to augment Notch signaling under hypoxic conditions. Vasorin promotes tumor growth and reduces survival in mouse models of glioblastoma, and its expression correlates with increased aggression of human gliomas. These findings provide mechanistic insights into how hypoxia promotes Notch signaling in glioma and identify Vasorin as a potential therapeutic target.