Scientific evidence suggests that pain contributes to the maintenance of tobacco cigarette smoking among individuals with varying levels of pain. Yet, little is understood about factors that may moderate relations between pain severity and smoking processes. Considering that women are more likely to experience deleterious pain- and smoking-related outcomes, female smokers may be a particularly vulnerable group when considering pain in the maintenance of maladaptive smoking behavior. Thus, it is important to investigate the role of sex in pain-smoking relations. The current cross-sectional study examined sex differences in the relation between reported levels of pain and cessation-relevant smoking processes (i.e. cigarette dependence, barriers for cessation, and past cessation-related problems). Participants included 100 adult daily cigarette smokers (M = 32.57 years, SD = 13.58; 33% female). Results indicated that greater pain was significantly associated with greater cigarette dependence, greater perceived barriers to cessation, and greater cessation-related problems among female, but not male, smokers. The current findings identify sex as a potentially important moderator of complex associations between pain and tobacco smoking and suggests that women may constitute a group that is especially vulnerable to the effects of pain in the maintenance of tobacco dependence. Based on the present data, integrated pain-smoking treatments may be especially useful for female, versus male, smokers.
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http://dx.doi.org/10.1016/j.addbeh.2018.11.007 | DOI Listing |
Proc Natl Acad Sci U S A
January 2025
Bioelectricity Laboratory, Department of Physiology and Biophysics, School of Medicine, University of California, Irvine, CA 92697.
Loss-of-function sequence variants in , which encodes the voltage-gated potassium channel Kv1.1, cause Episodic Ataxia Type 1 (EA1) and epilepsy. Due to a paucity of drugs that directly rescue mutant Kv1.
View Article and Find Full Text PDFPain
February 2025
Department of Anesthesiology, Faculty of Medicine and Health Sciences, Université de Sherbrooke, Sherbrooke, QC, Canada.
Chronic pain is a pervasive and debilitating condition with increasing implications for public health, affecting millions of individuals worldwide. Despite its high prevalence, the underlying neural mechanisms and pathophysiology remain only partly understood. Since its introduction 35 years ago, brain diffusion magnetic resonance imaging (MRI) has emerged as a powerful tool to investigate changes in white matter microstructure and connectivity associated with chronic pain.
View Article and Find Full Text PDFJ Neurosurg Anesthesiol
November 2024
Department of Anesthesiology and Pain Medicine, University of Washington, Seattle, WA.
This systematic review aimed to identify and describe best practice for the intraoperative anesthetic management of patients undergoing emergent/urgent decompressive craniotomy or craniectomy for any indication. The PubMed, Scopus, EMBASE, and Cochrane databases were searched for articles related to urgent/emergent craniotomy/craniectomy for intracranial hypertension or brain herniation. Only articles focusing on intraoperative anesthetic management were included; those investigating surgical or intensive care unit management were excluded.
View Article and Find Full Text PDFProc Natl Acad Sci U S A
January 2025
Department of Psychological and Brain Sciences, Indiana University, Bloomington, IN 47405.
Dysregulation of GABAergic inhibition is associated with pathological pain. Consequently, enhancement of GABAergic transmission represents a potential analgesic strategy. However, therapeutic potential of current GABA agonists and modulators is limited by unwanted side effects.
View Article and Find Full Text PDFProc Natl Acad Sci U S A
January 2025
Department of Medical Neuroscience, SUSTech Center for Pain Medicine, School of Medicine, Southern University of Science and Technology, Shenzhen 518055, China.
Ubiquitin-proteasomal degradation of K/Cl cotransporter 2 (KCC2) in the ventral posteromedial nucleus (VPM) has been demonstrated to serve as a common mechanism by which the brain emerges from anesthesia and regains consciousness. Ubiquitin-proteasomal degradation of KCC2 during anesthesia is driven by E3 ligase Fbxl4. However, the mechanism by which ubiquitinated KCC2 is targeted to the proteasome has not been elucidated.
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