Utility of Facebook\u27s social connectedness index in modeling COVID-19 spread: Exponential random graph modeling study

BACKGROUND: The COVID-19 (the disease caused by the SARS-CoV-2 virus) pandemic has underscored the need for additional data, tools, and methods that can be used to combat emerging and existing public health concerns. Since March 2020, there has been substantial interest in using social media data to both understand and intervene in the pandemic. Researchers from many disciplines have recently found a relationship between COVID-19 and a new data set from Facebook called the Social Connectedness Index (SCI). OBJECTIVE: Building off this work, we seek to use the SCI to examine how social similarity of Missouri counties could explain similarities of COVID-19 cases over time. Additionally, we aim to add to the body of literature on the utility of the SCI by using a novel modeling technique. METHODS: In September 2020, we conducted this cross-sectional study using publicly available data to test the association between the SCI and COVID-19 spread in Missouri using exponential random graph models, which model relational data, and the outcome variable must be binary, representing the presence or absence of a relationship. In our model, this was the presence or absence of a highly correlated COVID-19 case count trajectory between two given counties in Missouri. Covariates included each county\u27s total population, percent rurality, and distance between each county pair. RESULTS: We found that all covariates were significantly associated with two counties having highly correlated COVID-19 case count trajectories. As the log of a county\u27s total population increased, the odds of two counties having highly correlated COVID-19 case count trajectories increased by 66% (odds ratio [OR] 1.66, 95% CI 1.43-1.92). As the percent of a county classified as rural increased, the odds of two counties having highly correlated COVID-19 case count trajectories increased by 1% (OR 1.01, 95% CI 1.00-1.01). As the distance (in miles) between two counties increased, the odds of two counties having highly correlated COVID-19 case count trajectories decreased by 43% (OR 0.57, 95% CI 0.43-0.77). Lastly, as the log of the SCI between two Missouri counties increased, the odds of those two counties having highly correlated COVID-19 case count trajectories significantly increased by 17% (OR 1.17, 95% CI 1.09-1.26). CONCLUSIONS: These results could suggest that two counties with a greater likelihood of sharing Facebook friendships means residents of those counties have a higher likelihood of sharing similar belief systems, in particular as they relate to COVID-19 and public health practices. Another possibility is that the SCI is picking up travel or movement data among county residents. This suggests the SCI is capturing a unique phenomenon relevant to COVID-19 and that it may be worth adding to other COVID-19 models. Additional research is needed to better understand what the SCI is capturing practically and what it means for public health policies and prevention practices

CD36 maintains the gastric mucosa and associates with gastric disease

The gastric epithelium is often exposed to injurious elements and failure of appropriate healing predisposes to ulcers, hemorrhage, and ultimately cancer. We examined the gastric function of CD36, a protein linked to disease and homeostasis. We used the tamoxifen model of gastric injury in mice null for Cd36 (Cd3

CD36 maintains the gastric mucosa and associates with gastric disease.

The gastric epithelium is often exposed to injurious elements and failure of appropriate healing predisposes to ulcers, hemorrhage, and ultimately cancer. We examined the gastric function of CD36, a protein linked to disease and homeostasis. We used the tamoxifen model of gastric injury in mice null for Cd36 (Cd36-/-), with Cd36 deletion in parietal cells (PC-Cd36-/-) or in endothelial cells (EC-Cd36-/-). CD36 expresses on corpus ECs, on PC basolateral membranes, and in gastrin and ghrelin cells. Stomachs of Cd36-/- mice have altered gland organization and secretion, more fibronectin, and inflammation. Tissue respiration and mitochondrial efficiency are reduced. Phospholipids increased and triglycerides decreased. Mucosal repair after injury is impaired in Cd36-/- and EC-Cd36-/-, not in PC-Cd36-/- mice, and is due to defect of progenitor differentiation to PCs, not of progenitor proliferation or mature PC dysfunction. Relevance to humans is explored in the Vanderbilt BioVu using PrediXcan that links genetically-determined gene expression to clinical phenotypes, which associates low CD36 mRNA with gastritis, gastric ulcer, and gastro-intestinal hemorrhage. A CD36 variant predicted to disrupt an enhancer site associates (p < 10-17) to death from gastro-intestinal hemorrhage in the UK Biobank. The findings support role of CD36 in gastric tissue repair, and its deletion associated with chronic diseases that can predispose to malignancy

Visceral obesity and insulin resistance associate with CD36 deletion in lymphatic endothelial cells

Disruption of lymphatic lipid transport is linked to obesity and type 2 diabetes (T2D), but regulation of lymphatic vessel function and its link to disease remain unclear. Here we show that intestinal lymphatic endothelial cells (LECs) have an increasing CD36 expression from lymphatic capillaries (lacteals) to collecting vessels, and that LEC CD36 regulates lymphatic integrity and optimizes lipid transport. Inducible deletion of CD36 in LECs in adult mice (Cd36(ΔLEC)) increases discontinuity of LEC VE-cadherin junctions in lacteals and collecting vessels. Cd36(ΔLEC) mice display slower transport of absorbed lipid, more permeable mesenteric lymphatics, accumulation of inflamed visceral fat and impaired glucose disposal. CD36 silencing in cultured LECs suppresses cell respiration, reduces VEGF-C-mediated VEGFR2/AKT phosphorylation and destabilizes VE-cadherin junctions. Thus, LEC CD36 optimizes lymphatic junctions and integrity of lymphatic lipid transport, and its loss in mice causes lymph leakage, visceral adiposity and glucose intolerance, phenotypes that increase risk of T2D