Mechanisms of Nicotine Addiction

Picciotto, Marina R.; Kenny, Paul J.

doi:10.1101/cshperspect.a039610

Cited by 78 publications

(60 citation statements)

References 144 publications

(178 reference statements)

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“…In the KEGG pathway analysis, the mechanism of nicotine addiction has been confirmed to be one of the main factors of lung cancer 46 . With regard to peroxisome proliferator‐activated receptors (PPAR) signaling pathway, a large number of clinical studies have shown that PPAR‐γ ligands can effectively control tumor progression by affecting a variety of cellular processes such as cell proliferation, apoptosis, angiogenesis, inflammation, and metastasis 47 .…”

Section: Discussionmentioning

confidence: 99%

Role of hemoglobin alpha and hemoglobin beta in non‐small‐cell lung cancer based on bioinformatics analysis

Kang

Qiu

Wang

et al. 2022

Molecular Carcinogenesis

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The differentially expressed genes (DEGs) were identified and screened differentially in non‐small‐cell lung cancer (NSCLC) using information from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus databases, and the correlation of DEGs in protein interaction, function, and pathway enrichment were analyzed to search for new biomarkers and potential therapeutic targets for NSCLC. Protein–protein interaction network (PPI) analysis showed that CDK1 and GNGT1 were the most significantly upregulated hub nodes, while FPR2 was the most significantly downregulated. Gene Ontology enrichment analysis showed that upregulated DEGs were significantly enriched in protein heterodimerization activity and other functions, while downregulated DEGs were enriched in functions such as heparin‐binding. Kyoto Encyclopedia of Genes and Genomes pathway analysis showed that upregulation of DEGs were significantly associated with neuroactive ligand‐receptor interaction pathways, while downregulation of DEGs were significantly associated with malaria pathways. According to the analysis results, we identified hemoglobin alpha (HBA) and hemoglobin beta (HBB) as the genes of interest for further study. Through tissue level and cell level experiments, we found that the expressions of HBA and HBB in NSCLC tissues were significantly lower than those in paracancerous tissues, and downregulation of HBA and HBB could significantly affect the proliferation ability of NSCLC cells. In addition, we also found that changes in HBA and HBB may affect NSCLC cells through the p38/MAPK pathway and JNK pathway, and ultimately affect the occurrence and development of NSCLC.

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Section: Discussionmentioning

confidence: 99%

Role of hemoglobin alpha and hemoglobin beta in non‐small‐cell lung cancer based on bioinformatics analysis

Kang

Qiu

Wang

et al. 2022

Molecular Carcinogenesis

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“…Sowohl die PTBS als auch Substanzkonsumstörungen (allgemein, speziell) zeichnet eine vielfältige genetische Basis aus, die je für sich eine besondere Vulnerabilität versus Resilienz unter definierten Umwelteinflüssen epigenetisch mitbestimmt ( PTBS : [ 48 , 81 , 122 , 137 , 170 ]; Substanzkonsumstörungen allgemein : [ 11 , 23 , 64 , 71 , 189 ]; Alkohol: [ 43 ] Nikotin : [ 148 ]; Cannabis : [ 131 ]; Psychostimulantien : [ 89 , 149 ]); Opiate : [ 24 , 202 ]). Die genetische Forschung hat bisher zur Koexistenz/Komorbidität von PTBS und definierten Substanzkonsumstörungen erst einige wenige Studien vorgelegt: Für die Koexistenz von PTBS und Alkoholabhängigkeit konnte in Zwillingsstudien eine hohe genetische Überlappung nachgewiesen werden.…”

Section: Genetische Und Epigenetische Faktoren Als Gemeinsame Basis V...unclassified

Zur Komorbidität von Posttraumatischer Belastungsstörung und Sucht in biopsychosozialer Perspektive

Kapfhammer

2021

Neuropsychiatr

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ZusammenfassungPosttraumatische Belastungsstörung und Substanzkonsumstörungen treten im medizinischen Versorgungssystem häufig koexistent auf. Ihre Komorbidität geht mit schwerwiegenderen akuten klinischen Symptombildern, mit zahlreichen, oft notfallmäßigen Hospitalisierungen und geringeren Behandlungserfolgen einher. Ihre Komorbidität trägt zu dramatisch ungünstigeren Verläufen auf allen biopsychosozialen Ebenen bei. Das Thema Komorbidität von PTBS und Sucht wird auf mehreren Ebenen untersucht: in den Perspektiven von Epidemiologie, Substanzkonsumstörung als Risikofaktor für Trauma und PTBS, Trauma und PTBS als Risikofaktor für Substanzkonsumstörung, neurobiologischen Konsequenzen einer Substanzkonsumstörung für die Neurobiologie von PTBS, gemeinsam geteilten Faktoren der Genetik/Epigenetik, Persönlichkeitsdimensionen und aversiven/traumatogenen Einflüssen in der frühen Entwicklung. Der Hauptfokus der Analyse liegt auf den wechselseitig sich verstärkenden Mechanismen, die der Entwicklung und dem Verlauf beider Störungsbilder inhärent sind.

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“…Ethical approval: All applicable international, national, and/or institutional guidelines for the care and use of animals were followed. (1) and differences in brain glucose metabolism between rat strains (2). Type of change (↑ increase, ↓ decrease), ROI: region of interest, Side (L: left, R: right), t-value (T), statistical p-value (p) (uncorrected and corrected for multiple comparisons, FWE) at peak and cluster level, k (cluster size in number of voxels).…”

Section: Compliance With Ethical Standardsmentioning

confidence: 99%

“…Addiction vulnerability is the individual's risk of developing an addiction during their lifetime. Clinical and preclinical studies have shown that among the biological factors involved in this disorder, genetic variability plays an important role in humans [1][2][3][4] , accounting for at least 40-60% of the variation in vulnerability to drug dependence 5 . In this regard, the use of inbred rats has proven to be a valuable tool for identifying differences in vulnerability to drug addiction.…”

Section: Introductionmentioning

confidence: 99%

Neuroimaging Reveals Distinct Brain Glucose Metabolism Patterns Associated with Morphine Consumption in Two Inbreed Rat Models

Soto-Montenegro

García

Lamanna-Rama

et al. 2021

Preprint

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Addiction vulnerability is the individual's risk of developing an addiction during their lifetime. A challenge in the neurobiology of drug addiction is understanding why some people become addicted to drugs. Here, we used positron emission tomography (PET) and statistical parametric mapping (SPM) to evaluate changes in brain glucose metabolism in response to chronic morphine self-administration (MSA) in two rat strains with different vulnerability to drug abuse, Lewis (LEW) and Fischer 344 (F344). Four groups of animals were trained to self-administer morphine or saline for 15 days. 2-deoxy-2-[18F]-fluoro-D-glucose (FDG)-PET studies were performed on the last day of MSA (acquisition phase) and after 15 days of withdrawal. PET data were analyzed using SPM12. LEW-animals self-administered more morphine injections per session than F344-animals. We found significant brain metabolic differences between LEW and F344 strains in the cortex, hypothalamus, brainstem, and cerebellum. In addition, the different brain metabolic patterns observed after the MSA study between these rat strains indicate differences in the efficiency of neural substrates to translate the drug effects, which could explain the differences in predisposition to morphine abuse between one individual and another. These findings have important implications for the use of these rat strains in translational morphine and opiate research.

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Mechanisms of Nicotine Addiction

Cited by 78 publications

References 144 publications

Role of hemoglobin alpha and hemoglobin beta in non‐small‐cell lung cancer based on bioinformatics analysis

Role of hemoglobin alpha and hemoglobin beta in non‐small‐cell lung cancer based on bioinformatics analysis

Zur Komorbidität von Posttraumatischer Belastungsstörung und Sucht in biopsychosozialer Perspektive

Neuroimaging Reveals Distinct Brain Glucose Metabolism Patterns Associated with Morphine Consumption in Two Inbreed Rat Models

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