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Open Access Publications from the University of California

Recent Work

Tobacco use remains the single most preventable cause of disease, disability, and death in the United States and in California. The Tobacco-Related Disease Research Program (TRDRP) is one of three entities that constitute California’s program to control tobacco consumption and alleviate the burden of tobacco-related disease. This effort was initiated by Proposition 99, “The Tobacco Tax and Health Protection Act of 1988” which mandated that the Department of Health Services, the Department of Education and the University of California be allocated a portion of the tobacco tax revenue collected to address issues of tobacco consumption and its consequences in the state. Enabling legislation requested that the University of California, in its role as the research arm of the state, “administer a comprehensive grant program to support research efforts related to the prevention, causes, and treatment of tobacco-related diseases” and that “ all qualified investigators, regardless of institutional affiliation, shall have equal access and opportunity to compete for the funds.”

The TRDRP is administered by the University of California and is a program of the Research Grants Program Office (RGPO), Office of Research and Graduate Studies at the University of California, Office of the President.

Cover page of Smoking Cessation Interventions After Lung Cancer Screening Guideline Change

Smoking Cessation Interventions After Lung Cancer Screening Guideline Change


Introduction: Recent guideline changes for lung cancer screening with low-dose computed tomography recommend smoking cessation interventions be done in parallel with screening. The purpose of this study is to determine the post-guideline rates of smoking cessation interventions among patients eligible and ineligible for lung cancer screening.

Methods: Using electronic health records collected from a large ambulatory care system in northern California between 2010 and 2017, authors identified new patients who were current smokers aged 55–80 years visiting a primary care provider, and grouped patients into lung cancer screening–eligible heavy smokers, screening-ineligible moderate smokers, and screening-ineligible light smokers. Screening-eligible smokers versus screening-ineligible smokers were compared in receipt of smoking cessation interventions before (2010–2013) and after (2014–2017) the guideline change, overall and by intervention type (formal counseling, informal counseling, pharmacotherapy) using hierarchical generalized linear models. Analyses were conducted in 2018–2019.

Results: After the guideline change, the likelihood of receiving any smoking cessation intervention (OR=1.44, 95% CI=1.28, 1.61, p<0.05), informal counseling (OR=1.29, 95% CI=1.15, 1.46, p<0.05), and pharmacotherapy (OR=1.24, 95% CI=1.02, 1.50, p<0.05) during a new patient visit significantly increased, with the increase not varying by level of smoking. For formal counseling, the post-guideline increase was greater for screening-eligible heavy smokers (OR=3.15, 95% CI=1.18, 8.36, p<0.05) and moderate smokers (OR=3.58, 95% CI=1.29, 9.95, p<0.05) relative to light smokers.

Conclusions: Smoking cessation interventions increased after new lung cancer screening guidelines. Given the sizable adverse impacts of smoking on morbidity and mortality, small increases in implementation of smoking cessation interventions could have substantial public health benefits.

Cover page of G protein-coupled receptors activate p38 MAPK via a non-canonical TAB1-TAB2- and TAB1-TAB3-dependent pathway in endothelial cells.

G protein-coupled receptors activate p38 MAPK via a non-canonical TAB1-TAB2- and TAB1-TAB3-dependent pathway in endothelial cells.


Endothelial dysfunction is induced by inflammatory mediators including multiple G protein-coupled receptor (GPCR) agonists. However, the GPCR signaling pathways that promote endothelial dysfunction are incompletely understood. We previously showed that thrombin promotes endothelial barrier disruption through autophosphorylation and activation of p38 mitogen-activated protein kinase (MAPK) via a non-canonical transforming growth factor-β-activated protein kinase-1-binding protein-1 (TAB1) and TAB2-dependent pathway rather than the canonical three-tiered kinase cascade. Here, we sought to determine whether other GPCR agonists stimulate p38 MAPK activation via this non-canonical pathway in human endothelial cells derived from different vascular beds. Using primary human umbilical vein endothelial cells (HUVECs), HUVEC-derived EA.hy926 cells, and human dermal microvascular endothelial cells (HDMECs), we found that both non-canonical and canonical p38 activation pathways components are expressed in these various endothelial cell types, including TAB3, a structurally-related TAB2 homolog. Moreover, multiple GPCRs agonists, including thrombin, histamine, prostaglandin E2, and ADP, stimulated robust p38 autophosphorylation, whereas phosphorylation of the upstream MAPKs MAP kinase kinase 3 (MKK3) and MKK6, was virtually undetectable, indicating that non-canonical p38 activation may exist for other GPCRs. Indeed, in EA.hy926 cells, thrombin- and histamine-stimulated p38 activation depended on TAB1-TAB2, whereas in primary HUVECs, both TAB1-TAB2 and TAB1-TAB3 were required for p38 activation. In HDMECs, thrombin-induced p38 activation depended on TAB1-TAB3, but histamine-induced p38 activation required TAB1-TAB2. Moreover, thrombin- and histamine-stimulated interleukin-6 production required both TAB1-TAB2 and TAB1-TAB3 in HUVEC. We conclude that multiple GPCR agonists utilize non-canonical TAB1-TAB2 and TAB1-TAB3-dependent p38 activation to promote endothelial inflammatory responses.