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1.
Trauma Violence Abuse ; 24(3): 1818-1831, 2023 07.
Article in English | MEDLINE | ID: mdl-35446743

ABSTRACT

The Asian American, Native Hawaiian, and Pacific Islander (AANHPI) population is rapidly growing in the United States. Despite sexual violence being a persistent and significant public health issue, research on this topic among AANHPIs is lacking. The study objective is to conduct a systematic scoping review on the published literature on non-partner sexual violence among AANHPIs to identify gaps and priorities to inform actionable research. The systematic review was conducted following the PRISMA Protocol for Systematic Reviews. Database searches were conducted of MEDLINE, Embase, PsycINFO, and Cochrane Central of Clinical Trials, along with and AgeLine and CINAHL for peer-reviewed articles describing non-partner sexual violence among AANHPIs. The search was limited to articles in English published after 1990. Each citation was reviewed by two trained independent reviewers, with a third researcher resolving any conflicts. Of the 998 articles screened and subsequently 496 full-text articles assessed for eligibility, 38 articles were included in the final analysis. The majority of studies did not report disaggregated data for AANHPI subgroups, with most focusing on East Asian subgroups and little evidence on NHPI communities. Most studies were cross-sectional, quantitative, and employed non-probability sampling. There was a lack of studies on effectiveness of interventions and validity of sexual violence-related measures. Our review provides a first step in mapping the extant literature on non-partner sexual violence among this underserved and under-researched population and will serve as a guide for future research, policy, and intervention.


Subject(s)
Asian , Native Hawaiian or Other Pacific Islander , Sex Offenses , Adult , Humans , Pacific Island People , Sex Offenses/ethnology , United States
2.
Neuroscience ; 450: 126-134, 2020 12 01.
Article in English | MEDLINE | ID: mdl-32540365

ABSTRACT

Unpleasant somatosensory stimuli such as pain and itch can interrupt normal behavior. But survival can depend on resuming normal behavior before these challenges are fully resolved. The neural mechanisms that prioritize behavior when individuals are challenged with unpleasant somatosensory sensations, however, are not fully understood. Recently, we identified a neural circuit activated by hunger that can inhibit pain, prioritizing food seeking over tending to an injury. Here, we examine the ability of hunger, and neurons activated by hunger, to inhibit behavioral responses to another unpleasant somatosensory sensation - itch. We demonstrate that food deprivation inhibits scratching induced by three different pruritogenic stimuli: histamine, serotonin, and chloroquine. The inhibition of scratching correlates with the level of food deprivation, suggesting a cross-competition of alarm systems in the brain whereby more energy need more efficiently inhibits competing drives. Finally, we show that activity in hunger-sensitive, hypothalamic agouti-related protein (AgRP)-expressing neurons is sufficient to inhibit itch. Taken together, we showed that hunger or AgRP neuron activity inhibits itch, demonstrating that organisms have neural systems to filter and process ascending spinal signals activated by unpleasant somatosensory stimuli to prioritize salient needs.


Subject(s)
Hunger , Neurons , Agouti-Related Protein/metabolism , Food Deprivation , Humans , Hypothalamus/metabolism , Neurons/metabolism
3.
Neuron ; 103(5): 891-908.e6, 2019 09 04.
Article in English | MEDLINE | ID: mdl-31277924

ABSTRACT

Motivated behavior is influenced by neural networks that integrate physiological needs. Here, we describe coordinated regulation of hypothalamic feeding and midbrain reward circuits in awake behaving mice. We find that alcohol and other non-nutritive drugs inhibit activity in hypothalamic feeding neurons. Interestingly, nutrients and drugs utilize different pathways for the inhibition of hypothalamic neuron activity, as alcohol signals hypothalamic neurons in a vagal-independent manner, while fat and satiation signals require the vagus nerve. Concomitantly, nutrients, alcohol, and drugs also increase midbrain dopamine signaling. We provide evidence that these changes are interdependent, as modulation of either hypothalamic neurons or midbrain dopamine signaling influences reward-evoked activity changes in the other population. Taken together, our results demonstrate that (1) food and drugs can engage at least two peripheral→central pathways to influence hypothalamic neuron activity, and (2) hypothalamic and dopamine circuits interact in response to rewards.


Subject(s)
Central Nervous System Depressants/pharmacology , Dopamine Uptake Inhibitors/pharmacology , Dopaminergic Neurons/drug effects , Ethanol/pharmacology , Feeding Behavior/drug effects , Hypothalamus/drug effects , Nicotinic Agonists/pharmacology , Reward , Agouti-Related Protein/metabolism , Amphetamine/pharmacology , Animals , Cocaine/pharmacology , Dopamine Antagonists/pharmacology , Dopaminergic Neurons/metabolism , Hypothalamus/metabolism , Mice , Neural Pathways/drug effects , Neurons/drug effects , Neurons/metabolism , Nicotine/pharmacology , Pro-Opiomelanocortin/metabolism , Vagotomy , Vagus Nerve/physiology
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