Publications

BACKGROUND

Controversy exists regarding the safety of electrical stun guns (TASERs). Much of the research on TASERs is funded by the maker of the device and, therefore, could be biased. We sought to determine if funding source or author affiliation is associated with TASER research conclusions.

METHODS

MEDLINE was searched for TASER or electrical stun gun to identify relevant studies. All human and animal studies published up to September 01, 2010, were included. Reviews, editorials, letters, and case reports were excluded from the analysis. Two independent reviewers blinded to this study hypothesis evaluated each article with regard to conclusions of TASER safety.

RESULTS

Fifty studies were reviewed: 32 (64%) were human studies and 18 (36%) were animal studies. Twenty-three (46%) studies were funded by TASER International or written by an author affiliated with the company. Of these, 22 (96%) concluded that TASERs are unlikely harmful (26%) or not harmful (70%). In contrast, of the 22 studies not affiliated with TASER, 15 (55%) concluded that TASERs are unlikely harmful (29%) or not harmful (26%). A study with any affiliation with TASER International had nearly 18 times higher odds to conclude that the TASER is likely safe as compared with studies without such affiliation (odds ratio 17.6, 95% CI 2.1-150.1, P = .001).

CONCLUSIONS

Studies funded by TASER and/or written by an author affiliated with the company are substantially more likely to conclude that TASERs are safe. Research supported by TASER International may thus be significantly biased in favor of TASER safety.

Reduced bone morphogenetic protein receptor 2 (BMPR2) expression in patients with pulmonary arterial hypertension (PAH) can impair pulmonary arterial EC (PAEC) function. This can adversely affect EC survival and promote SMC proliferation. We hypothesized that interventions to normalize expression of genes that are targets of BMPR2 signaling could restore PAEC function and prevent or reverse PAH. Here we have characterized, in human PAECs, a BMPR2-mediated transcriptional complex between PPARγ and β-catenin and shown that disruption of this complex impaired BMP-mediated PAEC survival. Using whole genome-wide ChIP-Chip promoter analysis and gene expression microarrays, we delineated PPARγ/β-catenin-dependent transcription of target genes including APLN, which encodes apelin. We documented reduced PAEC expression of apelin in PAH patients versus controls. In cell culture experiments, we showed that apelin-deficient PAECs were prone to apoptosis and promoted pulmonary arterial SMC (PASMC) proliferation. Conversely, we established that apelin, like BMPR2 ligands, suppressed proliferation and induced apoptosis of PASMCs. Consistent with these functions, administration of apelin reversed PAH in mice with reduced production of apelin resulting from deletion of PPARγ in ECs. Taken together, our findings suggest that apelin could be effective in treating PAH by rescuing BMPR2 and PAEC dysfunction.