Child commercial sexual exploitation and sex trafficking are global health problems requiring a multidisciplinary approach by individuals, organizations, communities, and national governments. The adverse emotional, physical, and social consequences for victims are legion and in many areas of the United States and the rest of the world, victim resources are scarce. Since violence, deprivation, abuse, and infection are so integral to the exploitation experience, victims may present for care to community and academic pediatric and adolescent health care providers. It is essential that medical professionals have the knowledge, skills, and resources to recognize victims, assess their needs, and treat them appropriately, including making key referrals for community services. However, to date medical information and resources regarding commercial sexual exploitation and sex trafficking has been sparse. There are no clinically validated screening tools specifically designed to identify victims in the health care setting and since victims seldom self-identify, it is likely that the majority of victims are unrecognized. The opportunity for comprehensive assessment and intervention is lost. Further, professionals receive little training on appropriate interview techniques for this special population, and many are ill equipped to ensure safety and optimal medical evaluation during the visit. This article provides a general overview of child sex trafficking and commercial sexual exploitation (CSEC), describing the epidemiology of international and domestic exploitation, and reviewing the challenges of conducting research on this population. The five stages of trafficking are explained, as are typical physical and emotional consequences of exploitation. The medical evaluation is described, including potential indicators of CSEC and sex trafficking, common medical presentations by victims, approaches to the comprehensive medical interview, and the appropriate medical exam with diagnostic testing and treatment. Finally, a discussion of common victim needs is provided, with a description of resources and referrals.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1016/j.cppeds.2014.07.001 | DOI Listing |
J Am Soc Nephrol
January 2025
Research Program for Clinical and Molecular Metabolism, Faculty of Medicine, University of Helsinki, Helsinki, Finland.
Background: Deficiency of adiponectin and its downstream signaling may contribute to the pathogenesis of kidney injury in type 2 diabetes. Adiponectin activates intracellular signaling via adiponectin receptors 1 and 2 (AdipoR1 and AdipoR2), but the role of AdipoR-mediated signaling in glomerular injury in type 2 diabetes remains unknown.
Methods: The expression of AdipoR1 in the kidneys of people with type 2 diabetes and the expression of podocyte proteins or injury markers in the kidneys of AdipoR1-knockout (AdipoR1-KO) mice and immortalized AdipoR1-deficient human podocytes were investigated by immunohistochemistry and immunoblotting.
Nat Methods
January 2025
Broad Institute of MIT and Harvard, Cambridge, MA, USA.
A key challenge of the modern genomics era is developing empirical data-driven representations of gene function. Here we present the first unbiased morphology-based genome-wide perturbation atlas in human cells, containing three genome-wide genotype-phenotype maps comprising CRISPR-Cas9-based knockouts of >20,000 genes in >30 million cells. Our optical pooled cell profiling platform (PERISCOPE) combines a destainable high-dimensional phenotyping panel (based on Cell Painting) with optical sequencing of molecular barcodes and a scalable open-source analysis pipeline to facilitate massively parallel screening of pooled perturbation libraries.
View Article and Find Full Text PDFToxicology
January 2025
National Institute of Health Doutor Ricardo Jorge, I.P (INSA), Department of Human Genetics, Lisbon, Portugal; (b)Centre for Toxicogenomics and Human Health (ToxOmics), NOVA Medical School, Universidade NOVA de Lisboa, Lisbon, Portugal. Electronic address:
Understanding the potential impact of nanomaterials (NMs) on human health requires further investigation into the organ-specific nano-bio interplay at the cellular and molecular levels. We showed increased chromosomal damage in intestinal cells exposed to some of in vitro digested Titanium dioxide (TiO) NMs. The present study aimed to explore possible mechanisms linked to the uptake, epithelial barrier integrity, cellular trafficking, as well as activation of pro-inflammatory pathways, after exposure to three TiO-NMs (NM-102, NM-103, and NM-105).
View Article and Find Full Text PDFProc Natl Acad Sci U S A
February 2025
Department of Physiology and Membrane Biology, University of California Davis, Davis, CA 95616.
The L-type Ca channel (Ca1.2) is essential for cardiac excitation-contraction coupling. To contribute to the inward Ca flux that drives Ca-induced-Ca-release, Ca1.
View Article and Find Full Text PDFJ Cell Biol
April 2025
Department of Genetics and Cell Biology, College of Life Sciences, State Key Laboratory of Medicinal Chemical Biology, Nankai University, Tianjin, China.
TBC1D20 deficiency causes Warburg Micro Syndrome in humans, characterized by multiple eye abnormalities, severe intellectual disability, and abnormal sexual development, but the molecular mechanisms remain unknown. Here, we identify TBC1D20 as a novel Rab11 GTPase-activating protein that coordinates vesicle transport and actin remodeling to regulate ciliogenesis. Depletion of TBC1D20 promotes Rab11 vesicle accumulation and actin deconstruction around the centrosome, facilitating the initiation of ciliogenesis even in cycling cells.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!