The impact of the Oakland sugar-sweetened beverage tax on price promotions of sugar-sweetened and alternative beverages.

The goal of sugar-sweetened beverage (SSB) taxes is to raise the prices of SSBs to decrease consumption. Price promotions play an important role in the sales of SSBs and could potentially be used by manufacturers to weaken the impact of such taxes. The purpose of this study is to determine how price promotions changed after the introduction of the 2017 Oakland SSB tax. A difference-in-differences study design was used to compare changes in prices and the prevalence and amount of price promotions for beverages in Oakland, California, relative to Sacramento, California, using two different datasets. Nielsen Retail Scanner data included price promotions for beverages sold and store audit data included price promotions offered by retailers. Changes were analyzed for SSBs, noncalorically sweetened beverages, and unsweetened beverages. After the implementation of the tax, the prevalence of price promotions for SSBs did not change significantly in Oakland relative to the comparison site of Sacramento. However, the depth of price promotions increased by an estimated 0.35 cents per ounce (P<0.001) based on the Nielsen retail scanner data and by 0.39 cents per ounce (P<0.001) based on the store audit data. This increase in the amount by which SSBs were price promoted following the introduction of the Oakland SSB tax may reflect a strategy by manufacturers to weaken the tax and/or retailers to bolster demand.

An Assessment of Food Store Compliance With the Cook County Sweetened Beverage Tax.

To examine the correct application of the $0.01/ounce Cook County, Illinois, Sweetened Beverage Tax on sugar-sweetened and artificially sweetened beverages, a total of 111 beverage products were purchased from 28 food stores in September and November 2017. Purchases were categorized by taxable (sugar-sweetened and artificially sweetened soda and juice drinks) and nontaxable (100% fruit juice and sparkling water) beverage type, store type (limited service vs supermarket/grocery), and area median household income (lower vs higher). Two-sample tests of proportions were conducted to compare correctly taxed purchases. The tax was correctly applied in 91.0% of cases. Correct tax application was found in 87.8% of taxable beverage purchases versus 97.3% of nontaxable beverage purchases (P = .10), 71.4% of juice drink purchases versus 95.6% of nonjuice drink purchases (P < .001), and 85.5% of limited service store purchases versus 100% of supermarket/grocery purchases (P = .01). No significant differences were found by area income.

Intact Toll-like receptor 9 signaling in neutrophils modulates normal thrombogenesis in mice.

BACKGROUND: Deletion of Toll-like receptor 9 (Tlr9) signaling, which is important for sterile inflammatory processes, results in impaired resolution of venous thrombosis (VT) in mice. The purpose of this study was to determine if deletion of Tlr9 affected sterile necrosis, apoptosis, and neutrophil extracellular trap (NET) production in VT. METHODS: Stasis and nonstasis murine models of VT were used in wild-type (WT) and Tlr9-/- mice, with assessment of thrombus size and determination of NETs, necrosis, and apoptosis markers. Anti-polymorphonuclear neutrophil (PMN) and antiplatelet antibody strategies were used to determine the cellular roles and their roles in WT and Tlr9-/- mice. RESULTS: At 2 days, stasis thrombi in Tlr9-/- mice were 62% larger (n = 6-10), with 1.4-fold increased uric acid levels, 1.7-fold more apoptotic cells, 2-fold increased citrullinated histones, 2-fold increased peptidylarginine deiminase 4 (PAD4), and 1.5-fold increased elastase and a 2.4-fold reduction in tissue factor pathway inhibitor compared with WT mice (all n = 4-7; P < .05). In contrast, the sizes of nonstasis thrombi were not significantly different in Tlr9-/- mice (n = 4-6), and they did not have elevated necrosis or NET markers. Stasis thrombus size was not reduced at the 2-day time point in WT or Tlr9-/- mice that received treatment with deoxyribonuclease I or in PAD4-/- mice, which are incapable of forming NETs. In Tlr9-/- mice undergoing PMN depletion (n = 8-10), stasis thrombus size was reduced 18% and was associated with 29-fold decreased citrullinated histones, 1.3-fold decreased elastase, and 1.5-fold increased tissue factor pathway inhibitor (all n = 6; P < .05). Last, platelet depletion (>90% reduction) did not significantly reduce stasis thrombus size in Tlr9-/- mice. CONCLUSIONS: These data suggest that the thrombogenic model affects Tlr9 thrombogenic mechanisms and that functional Tlr9 signaling in PMNs, but not in platelets or NETs, is an important mechanism in early stasis experimental venous thrombogenesis.

Divergent effects of Tlr9 deletion in experimental late venous thrombosis resolution and vein wall injury.

Deep-vein thrombosis (DVT) resolves via a sterile inflammatory response. Defining the inflammatory response of DVT may allow for new therapies that do not involve anticoagulation. Previously, we have shown that Toll-like receptor 9 (Tlr9) gene deleted mice had impaired venous thrombosis (VT) resolution. Here, we further characterise the role of Tlr9 signalling and sterile inflammation in chronic VT and vein wall responses. First, we found a human precedent exists with Tlr9+ cells present in chronic post thrombotic intraluminal tissue. Second, in a stasis VT mouse model, endogenous danger signal mediators of uric acid, HMGB-1, and neutrophil extracellular traps marker of citrullinated histone-3 (and extracellular DNA) were greater in Tlr9-/- thrombi as compared with wild-type (WT), corresponding with larger VT at 8 and 21 days. Fewer M1 type (CCR2+) monocyte/macrophages (MØ) were present in Tlr9-/- thrombi than WT controls at 8 days, suggesting an impaired inflammatory cell influx. Using bone marrow-derived monocyte (BMMØ) cell culture, we found decreased fibrinolytic gene expression with exposure to several endogenous danger signals. Next, adoptive transfer of cultured Tlr9+/+ BMMØ to Tlr9-/- mice normalised VT resolution at 8 days. Lastly, although the VT size was larger at 21 days in Tlr9-/- mice and correlated with decreased endothelial antigen markers, no difference in fibrosis was found. These data suggest that Tlr9 signalling in MØ is critical for later VT resolution, is associated with necrosis clearance, but does not affect later vein wall fibrosis. These findings provide insight into the Tlr9 MØ mechanisms of sterile inflammation in this disease process.

Dobutamine-induced eosinophilia.

A man with dilated cardiomyopathy presented with decompensated heart failure and marked eosinophilia. After extensive clinical and laboratory evaluation for hypereosinophilic syndrome, including a myocardial biopsy, it was determined by means of rechallenge (second dobutamine infusion) that the patient was afflicted with dobutamine-induced eosinophilia. This report is important because of the high utilization rate of this drug in a sick population. Simply discontinuing it or switching to another agent can avert the high cost and risk of the evaluation for hypereosinophilic syndrome in this compromised group of patients.