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Background Home healthcare workers (HHWs) provide medical and nonmedical services to home‐bound patients. They are at great risk of experiencing violence perpetrated by patients (type II violence). Establishing the reliable prevalence of such violence and identifying vulnerable subgroups are essential in enhancing HHWs’ safety. We, therefore, conducted meta‐analyses to synthesize the evidence for prevalence and identify vulnerable subgroups. Methods Five electronic databases were searched for journal articles published between 1 January 2005 and 20 March 2019. A total of 21 studies were identified for this study. Meta‐analyses of prevalence were conducted to obtain pooled estimates. Meta‐regression was performed to compare the prevalence between professionals and paraprofessionals. Results Prevalence estimates for HHWs were 0.223 for 12 months and 0.302 for over the career for combined violence types, 0.102 and 0.171, respectively, for physical violence, and 0.364 and 0.418, respectively, for nonphysical violence. The prevalence of nonphysical violence was higher than that of physical violence for professionals in 12 months (0.515 vs 0.135) and over the career (0.498 vs 0.224) and for paraprofessionals in 12 months (0.248 vs 0.086) and over the career (0.349 vs 0.113). Professionals reported significantly higher nonphysical violence for 12‐month prevalence than paraprofessionals did (0.515 vs 0.248, P = .015). Conclusion A considerable percentage of HHWs experience type II violence with higher prevalence among professionals. Further studies need to explore factors that can explain the differences in the prevalence between professionals and paraprofessionals. The findings provide support for the need for greater recognition of the violence hazard in the home healthcare workplace.

Sphingosine 1‐phosphate (S1P), a sphingolipid released from activated platelets, stimulates COX‐2 induction. S1P activates GPCRs coupled to Gα family members. This study investigated whether Gα12 family regulates COX‐2 induction by S1P and if so, what the molecular basis is for its COX‐2 regulation. Gene knockout or chemical inhibitor experiments revealed that S1P induction of COX‐2 requires Gα12, but not Gα13, Gαq or Gαi/o. The specific role of Gα12 in COX‐2 induction by S1P was verified by promoter luciferase assay, Gα12 transfection and siRNA experiments. Absence of Gα12 inhibited NF‐κB DNA binding activity. Immunocytochemistry, ChIP and NF‐κB site mutation analyses confirmed the functional role of NF‐κB in COX‐2 gene transcription by S1P. Gα12 deficiency unaffected S1P‐mediated IκBα phosphorylation, but abrogated its ubiquitinylation and degradation, thereby abolishing p65 nuclear translocation. Chemical inhibition of S1P‐activated JNK abolished IκBα ubiquitinylation by S1P. Consistently, JNK transfection caused S1P to degrade IκBα during Gα12 deficiency. S1P injection induced COX‐2 in the lungs and livers of mice with an increase in the plasma PGE2, which was prevented by Gα12 gene knockout. Of the Gα proteins coupled to S1P receptors, Gα12 specifically regulates NF‐κB‐mediated COX‐2 induction by S1P, which is mediated by ubiquitinylation and degradation, but not phosphorylation, of IκBα.