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INTRODUCTION: Amid the successes of local sugar-sweetened beverage (SSB) taxes, interest in state-wide policies has grown. This study evaluated the cost effectiveness of a hypothetical 2-cent-per-ounce excise tax in California and its implications for population health and health equity. METHODS: Using the Childhood Obesity Intervention Cost-Effectiveness Study microsimulation model, tax impacts on health, health equity, and cost effectiveness over 10 years in California were projected, both overall and stratified by race/ethnicity and income. Expanding on previous models, differences in the effect of intake of SSBs on weight by BMI category were incorporated. Costing was performed in 2020, and analyses were conducted in 2021-2022. RESULTS: The tax is projected to save $4.55 billion in healthcare costs, prevent 266,000 obesity cases in 2032, and gain 114,000 quality-adjusted life years. Cost-effectiveness metrics, including cost/quality-adjusted life year gained, were cost saving. Spending on SSBs was projected to decrease by $33 per adult and $26 per child overall in the first year. Reductions in obesity prevalence for Black and Hispanic Californians were 1.8 times larger than for White Californians, and reductions for adults with lowest incomes (<130% Federal Poverty Level) were 1.4 times the reduction among those with highest incomes (>350% Federal Poverty Level). The tax is projected to save $112 in obesity-related healthcare costs per $1 invested. CONCLUSIONS: A state-wide SSB tax in California would be cost saving, lead to reductions in obesity and improvement in SSB-related health equity, and lead to overall improvements in population health. The policy would generate more than $1.6 billion in state tax revenue annually that can also be used to improve health equity.

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INTRODUCTION: Transcatheter Aortic Valve Replacement (TAVR) procedures at our institution were complicated by perioperative hypothermia despite use of the standard of care forced-air convective warming device (the BairHugger, Augustine Medical Inc, Eden Prairie, MN, USA). To remedy this problem, we initiated a quality improvement process that investigated the use of a conductive warm water-circulating device (the Allon ThermoWrap, Menen Medical Corporation, Trevose, PA, USA), and hypothesized that it would decrease the incidence of perioperative hypothermia. METHODS: We compared two different intraoperative warming devices using a historic control. We retrospectively reviewed intraoperative records of 80 TAVRs between 6/2013 and 6/2015, 46 and 34 of which were done with the forced-air and water-circulating devices, respectively. Continuous temperature data obtained from pulmonary artery catheter, temperature upon arrival to cardiothoracic ICU (CTU), age, BSA, height, and BMI were compared. RESULTS: Patients warmed with both devices were similar in terms of demographic characteristics. First recorded intraoperative temperature (mean 36.26 ± SD 0.61 vs. 35.95 ± 0.46°C, p = 0.02), lowest intraoperative temperature (36.01 ± 0.58 vs. 34.89 ± 0.76°C, p<0.001), temperature at the end of the procedure (36.47 ± 0.51 vs. 35.17 ± 0.75°C, p<0.001), and temperature upon arrival to the CTU (36.35 ± 0.44 vs. 35.07 ± 0.78°C, p<0.001) were significantly higher in the water-circulating group as compared to the forced-air group. CONCLUSION: A quality improvement process led to selection of a new warming device that virtually eliminated perioperative hypothermia at our institution. Patients warmed with the new device were significantly less likely to experience intraoperative hypothermia and were significantly more likely to be normothermic upon arrival to the CTU.

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Exposure to N-methyl-d-aspartate (NMDA) receptor antagonists has been demonstrated to induce neurodegeneration in newborn rats. However, in clinical practice the use of NMDA receptor antagonists as anesthetics and sedatives cannot always be avoided. The present study investigated the effect of the indirect cholinergic agonist physostigmine on neurotrophin expression and the extracellular matrix during NMDA receptor antagonist induced injury to the immature rat brain. The aim was to investigate matrix metalloproteinase (MMP)-2 activity, as well as expression of tissue inhibitor of metalloproteinase (TIMP)-2 and brain-derived neurotrophic factor (BDNF) after co-administration of the non-competitive NMDA receptor antagonist MK801 (dizocilpine) and the acetylcholinesterase (AChE) inhibitor physostigmine. The AChE inhibitor physostigmine ameliorated the MK801-induced reduction of BDNF mRNA and protein levels, reduced MK801-triggered MMP-2 activity and prevented decreased TIMP-2 mRNA expression. Our results indicate that AChE inhibition may prevent newborn rats from MK801-mediated brain damage by enhancing neurotrophin-associated signaling pathways and by modulating the extracellular matrix.

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Recently, a universal, simple, and fail-safe mechanism has been proposed by which cerebral blood flow (CBF) might be coupled to oxygen metabolism during neuronal activation without the need for any tissue-based mechanism. According to this concept, vasodilation occurs by local erythrocytic release of nitric oxide or ATP wherever and whenever hemoglobin is deoxygenated, directly matching oxygen demand and supply in every tissue. For neurovascular coupling in the brain, we present experimental evidence challenging this view by applying an experimental regime operating without deoxy-hemoglobin. Hyperbaric hyperoxygenation (HBO) allowed us to prevent hemoglobin deoxygenation, as the oxygen that was physically dissolved in the tissue was sufficient to support oxidative metabolism. Regional CBF and regional cerebral blood oxygenation were measured using a cranial window preparation in anesthetized rats. Hemodynamic and neuronal responses to electrical forepaw stimulation or cortical spreading depression (CSD) were analyzed under normobaric normoxia and during HBO up to 4 ATA (standard atmospheres absolute). Inconsistent with the proposed mechanism, during HBO, CBF responses to functional activation or CSD were unchanged. Our results show that activation-induced CBF regulation in the brain does not operate through the release of vasoactive mediators on hemoglobin deoxygenation or through a tissue-based oxygen-sensing mechanism.

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