Objectives: To examine the link between human trafficking of minors and childhood adversity.
Methods: We compared the prevalence of adverse childhood experiences (ACEs) and cumulative childhood adversity (ACE score) among a sample of 913 juvenile justice-involved boys and girls in Florida for whom the Florida child abuse hotline accepted human trafficking abuse reports between 2009 and 2015 with those of a matched sample.
Results: ACE composite scores were higher and 6 ACEs indicative of child maltreatment were more prevalent among youths who had human trafficking abuse reports. Sexual abuse was the strongest predictor of human trafficking: the odds of human trafficking was 2.52 times greater for girls who experienced sexual abuse, and there was a 8.21 times greater risk for boys who had histories of sexual abuse.
Conclusions: Maltreated youths are more susceptible to exploitation in human trafficking. Sexual abuse in connection with high ACE scores may serve as a key predictor of exploitation in human trafficking for both boys and girls.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5227932 | PMC |
| http://dx.doi.org/10.2105/AJPH.2016.303564 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Basic Science and Pathogenesis.
Alzheimers Dement
December 2024
Shenzhen Bay Laboratory, Shenzhen, Guandong, China.
Background: The classic mode of STING activation is through binding the cyclic dinucleotide 2'3'-cyclic GMP-AMP (cGAMP), produced by the DNA sensor cyclic GMP-AMP synthase (cGAS), which is important for the innate immune response to microbial infection and autoimmune disease. Modes of STING activation that are independent of cGAS are much less well understood. We wanted to explore the interactome of STING on the organelles during its trafficking route and to understand the regulatory network of STING signaling.
View Article and Find Full Text PDFBasic Science and Pathogenesis.
Alzheimers Dement
December 2024
Univ. Lille, Inserm, CHU Lille, Institut Pasteur de Lille, U1167-RID-AGE, DISTALZ, Lille, France.
Background: BIN1 is a major susceptibility gene for AD and BIN1 protein interacts with Tau. However, the contribution of BIN1 and its isoforms to AD pathogenesis remains unclear. We recently described that human BIN1 isoform1 (BIN1iso1) induces an accumulation of early endosome vesicles leading to neurodegeneration in Drosophila retina and that the early endosome size regulation was conserved in human induced neurons.
View Article and Find Full Text PDFBasic Science and Pathogenesis.
Alzheimers Dement
December 2024
Buck Institute for Research on Aging, Novato, CA, USA.
Background: Synapses can modify their strength in response to activity, and the unique properties of synapses that regulate their plasticity are essential for memory. Long-term potentiation (LTP) is considered the physiological basis for how neurons encode new memories. A complex series of postsynaptic signaling events in LTP is associated with memory deficits in tauopathy models, but the mechanism by which pathogenic tau inhibits plasticity at synapses is unknown.
View Article and Find Full Text PDFBasic Science and Pathogenesis.
Alzheimers Dement
December 2024
John P. Hussman Institute for Human Genomics, Miller School of Medicine, Miami, FL, USA.
Background: We identified the missense variant Ser1038Cys (rs377155188) in the tetratricopeptide repeat domain 3 (TTC3) gene that segregate in a non-Hispanic white late onset Alzheimer disease (LOAD) family. This variant is predicted to be deleterious and extremely rare (MAF<0.01%).
View Article and Find Full Text PDFBasic Science and Pathogenesis.
Alzheimers Dement
December 2024
Department of Neurology, Mayo Clinic, Rochester, MN, USA.
Background: Despite recent FDA approvement of disease-modifying treatments that reduce Aβ, the identification of novel therapeutic strategies that could delay the Alzheimer's disease (AD) development are needed. We identified and developed novel small molecule compounds that mildly inhibit mitochondrial complex I (MCI). Chronic treatment with a tool compound CP2 in 4 mouse models of familial AD was efficacious protecting against synaptic dysfunction and memory impairment, improving brain energetics and cognitive performance, reducing levels of human pTau and Ab.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!