Navigating Radiation Therapy During COVID-19 Using YouTube as a Source of Information.

The COVID-19 pandemic brought considerable change to the practice of radiotherapy. In the meantime, patients are increasingly turning to online resources for health information, with YouTube being one of the biggest platforms. However, little is known about what information is being disseminated to cancer patients about radiotherapy in the context of COVID-19. Therefore, this study aims to characterize and assess YouTube videos on radiotherapy during COVID-19. A YouTube search using the terms "Radiation therapy COVID-19", "Radiation therapy coronavirus", "Radiotherapy COVID-19", and "Radiotherapy coronavirus" was completed using a clear-cache web browser. The top 50 videos were collected from each search. After applying pre-determined exclusion criteria, each video was assessed for general parameters, source, and content. Two raters were used to ensure interrater reliability. One hundred five unique videos resulted from the four searches. Ninety-eight per cent were published in the last year. The median video length was 6 min and 54 s, and the median number of views was 570. Most videos were from the USA (58%). The majority of videos were published by a commercial channel (31%), non-profit organization (28%), or healthcare facility (26%). Forty-two per cent of the videos covered a topic related to radiotherapy during the pandemic. Bias was identified in 6% of videos. YouTube information on radiotherapy during COVID-19 is non-specific and can be misleading. The results of this study highlight the need for healthcare providers to proactively address patient information needs and guide them to appropriate sources of information.

Social and structural determinants of injection drug use-associated bacterial and fungal infections: A qualitative systematic review and thematic synthesis.

BACKGROUND AND AIMS: Injection drug use-associated bacterial and fungal infections are increasingly common, and social contexts shape individuals' injecting practices and treatment experiences. We sought to synthesize qualitative studies of social-structural factors influencing incidence and treatment of injecting-related infections. METHODS: We searched PubMed, EMBASE, Scopus, CINAHL and PsycINFO from 1 January 2000 to 18 February 2021. Informed by Rhodes' 'risk environment' framework, we performed thematic synthesis in three stages: (1) line-by-line coding; (2) organizing codes into descriptive themes, reflecting interpretations of study authors; and (3) consolidating descriptive themes into conceptual categories to identify higher-order analytical themes. RESULTS: We screened 4841 abstracts and included 26 qualitative studies on experiences of injecting-related bacterial and fungal infections. We identified six descriptive themes organized into two analytical themes. The first analytical theme, social production of risk, considered macro-environmental influences. Four descriptive themes highlighted pathways through which this occurs: (1) unregulated drug supply, leading to poor drug quality and solubility; (2) unsafe spaces, influenced by policing practices and insecure housing; (3) health-care policies and practices, leading to negative experiences that discourage access to care; and (4) restrictions on harm reduction programmes, including structural barriers to effective service provision. The second analytical theme, practices of care among people who use drugs, addressed protective strategies that people employ within infection risk environments. Associated descriptive themes were: (5) mutual care, including assisted-injecting and sharing sterile equipment; and (6) self-care, including vein health and self-treatment. Within constraining risk environments, some protective strategies for bacterial infections precipitated other health risks (e.g. HIV transmission). CONCLUSIONS: Injecting-related bacterial and fungal infections are shaped by modifiable social-structural factors, including poor quality unregulated drugs, criminalization and policing enforcement, insufficient housing, limited harm reduction services and harmful health-care practices. People who inject drugs navigate these barriers while attempting to protect themselves and their community.

Too much or too little information: how unknown uncertainty fuels time inconsistency.

Under uncertainty, there is considerable heterogeneity in expectations of results, and the outcome of each choice is a reflection of those expectations. This study aims to understand the role of subjective probabilistic inference in updating information for decision-making procedures under uncertainty. We show that adding uncertainty of trade-offs in decision-making criteria induces more inconsistent present preferences. We find that subjective probabilistic inference results in different levels of information acquisition, which plays a central role in many everyday cases of forecasting. The result of forecasting exerts substantive constraints on cognitive processes and shapes a type of restriction or stimulus in decision-making procedures. As uncertainty increases, generated fear of losses turns into an obstacle to the information acquisition process, and especially participants with low probabilistic inference tend to overestimate or underestimate future unknown rewards. In addition, our experiment shows that risk preference does not play a key role in decision-making procedures under unknown uncertainty. This finding is an experimental manifestation of Knight's argument (Risk, uncertainty, and profit, Houghton Mifflin, Boston, 1921), which explains unknown uncertainty, and shows the relationship between cognitive ability and time inconsistency. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s43546-021-00189-9.

Raloxifene prevents stress granule dissolution, impairs translational control and promotes cell death during hypoxia in glioblastoma cells.

Glioblastoma (GBM) is the most common primary malignant brain tumor, and it has a uniformly poor prognosis. Hypoxia is a feature of the GBM microenvironment, and previous work has shown that cancer cells residing in hypoxic regions resist treatment. Hypoxia can trigger the formation of stress granules (SGs), sites of mRNA triage that promote cell survival. A screen of 1120 FDA-approved drugs identified 129 candidates that delayed the dissolution of hypoxia-induced SGs following a return to normoxia. Amongst these candidates, the selective estrogen receptor modulator (SERM) raloxifene delayed SG dissolution in a dose-dependent manner. SG dissolution typically occurs by 15 min post-hypoxia, however pre-treatment of immortalized U251 and U3024 primary GBM cells with raloxifene prevented SG dissolution for up to 2 h. During this raloxifene-induced delay in SG dissolution, translational silencing was sustained, eIF2α remained phosphorylated and mTOR remained inactive. Despite its well-described role as a SERM, raloxifene-mediated delay in SG dissolution was unaffected by co-administration of ß-estradiol, nor did ß-estradiol alone have any effect on SGs. Importantly, the combination of raloxifene and hypoxia resulted in increased numbers of late apoptotic/necrotic cells. Raloxifene and hypoxia also demonstrated a block in late autophagy similar to the known autophagy inhibitor chloroquine (CQ). Genetic disruption of the SG-nucleating proteins G3BP1 and G3BP2 revealed that G3BP1 is required to sustain the raloxifene-mediated delay in SG dissolution. Together, these findings indicate that modulating the stress response can be used to exploit the hypoxic niche of GBM tumors, causing cell death by disrupting pro-survival stress responses and control of protein synthesis.

[Role of prostaglandins in colon cancer].

Colon cancer is one of the major leading causes of cancer-related deaths in the Western countries. In Korea, the incidence of colon cancer is increasing due to changes in environment and lifestyle such as diet. Chemoprevention strategy using non-steroidal anti-inflammatory drugs (NSAIDs) has been under intensive clinical and epidemiological research as these drugs suppress colorectal cancer. The best known targets of NSAIDs are cyclooxygenase (COX) enzymes, which convert arachidonic acid to prostaglandins (PGs) and thromboxane. Among these PGs, prostaglandin E2 (PGE2) can promote tumor growth by binding its receptors and activating signal pathways which control cell proliferation, migration, apoptosis, and angiogenesis. Therefore, COX inhibition is promising approach for chemoprevention of colorectal cancer. However, the prolonged use of COX-2 inhibitors is associated with unacceptable cardiovascular side effects. Thus, new targets involved in PGs metabolism are under investigation. 15-hydroxyprostaglandin dehydrogenase (15-PGDH), a key metabolic enzyme of PGE2, was up-regulated in normal colonic epithelium, but decreased in colon cancer. Recent findings suggest that 15-PGDH is involved in the neoplastic progression of initiated colonic epithelial cells. Also, new players related with PGs metabolism including prostaglandin transporter (PGT) and microsomal prostaglandin E synthase (mPGES) were reported to play a role in colorectal cancer development. This review presents current knowledge about the role of prostaglandins and associated proteins in colorectal cancer development and progression.