Substance use disorder (SUD) is common among victims of sex trafficking. Traffickers may exploit individuals' existing opioid use or other SUDs to coerce them into sex trafficking, or they may facilitate substance use to keep trafficking victims from exiting. Additionally, trafficking victims may use substances to cope with trauma. The intersections of sex trafficking and SUD complicate both legal responses and victim advocate responses to sex trafficking cases. Victim SUD can lead to challenges for law enforcement and prosecutors in developing cases against traffickers. On the provider side, traditional victim services are often insufficient for victims of trafficking with SUDs, who face substantial barriers to accessing services. A better understanding of the nexus between sex trafficking and SUDs is critical for implementing victim-centered and trauma-informed responses to this vulnerable population. In this article, the authors describe an online panel, convened in April 2021 by RTI International and the RAND Corporation on behalf of the National Institute of Justice, in which subject-matter experts and criminal justice practitioners discussed how SUDs and sex trafficking complicate the identification and screening of victims and victims' ability to access treatment and legal remedies. The panel participants identified 21 high-priority needs to support a better understanding of sex trafficking and SUDs and a variety of solutions for addressing these intertwined issues.
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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.
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