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Dataset results
884 results for “Nicotine”
Sex-specific transcriptomic profiles and imprinting drive nicotine self-administration in rats and inform the genetic basis of human smoking behavior
GEO Series GSE157683. Rattus norvegicus. 24 samples. Type: Expression profiling by high throughput sequencing.
Habenular Tcf7l2 links nicotine addiction to diabetes
GEO Series GSE137118. Rattus norvegicus. 36 samples. Type: Expression profiling by high throughput sequencing.
RNA-seq of iPSC-ECs treated e-cig liquids with and without nicotine
GEO Series GSE125217. Homo sapiens. 15 samples. Type: Expression profiling by high throughput sequencing.
Nickel-induced transcriptional memory in lung epithelial cells promotes interferon signaling upon nicotine exposure
GEO Series GSE242791. Homo sapiens. 12 samples. Type: Expression profiling by high throughput sequencing.
Single-Cell RNA-Sequencing of Human Embryonic Stem Cell Differentiation Delineates Adverse Effects of Nicotine on Embryonic Development
GEO Series GSE125416. Homo sapiens. 2 samples. Type: Expression profiling by high throughput sequencing.
The prenatal nicotine exposure leads to epigenetic alterations in nervous system signaling genes in the rat [RNA-seq]
GEO Series GSE253595. Rattus norvegicus. 6 samples. Type: Expression profiling by high throughput sequencing.
Beta arrestin1 associated genomic regions in nicotine induced Non-Small Cell Lung Carcinoma (NSCLC) cell line A549
GEO Series GSE40689. Homo sapiens. 3 samples. Type: Genome binding/occupancy profiling by high throughput sequencing.
Unveiling microbial dynamics in lung adenocarcinoma and adjacent nontumor tissues: Insights from nicotine exposure and diverse clinical stages via Nanopore Sequencing Technology
GEO Series GSE262090. metagenomes. 74 samples. Type: Other.
Alteration of gene expression profile of cerebelllar neuron-enriched cultures from neonatal rats by nicotine, acetamiprid, or imidacloprid treatment [nicotine]
GEO Series GSE80638. Rattus norvegicus. 12 samples. Type: Expression profiling by array.
Increased response to nicotine in human dopaminergic neurons derived from iPSC carrying the risk-associated SNP rs16969968
GEO Series GSE56398. Homo sapiens. 10 samples. Type: Expression profiling by high throughput sequencing.
The influence of adolescent nicotine exposure on ethanol intake brain gene expression
GEO Series GSE115188. Mus musculus. 16 samples. Type: Expression profiling by high throughput sequencing.
Effect of in utero nicotine exposure and elastase instillation on transcriptomic profile at post-elastase day 3 in mice
GEO Series GSE167567. Mus musculus. 14 samples. Type: Expression profiling by high throughput sequencing.
Transcriptomic Analysis of Nicotine on the Cardiovascular System Using a Diverse Population of Human Induced Pluripotent Stem Cell-derived Endothelial Cells
GEO Series GSE274506. Homo sapiens. 40 samples. Type: Expression profiling by high throughput sequencing.
Data from: Alcohol reduces muscle fatigue through atomistic interactions with nicotinic receptors
Alcohol consumption affects many organs and tissues, including skeletal muscle. However, the molecular mechanism of ethanol action on skeletal muscle remains unclear. Here, using molecular dynamics simulations and single channel recordings, we show that ethanol interacts with a negatively charged amino acid within an extracellular region of the neuromuscular nicotinic acetylcholine receptor (nAChR), thereby altering its global conformation and reducing the single channel current amplitude. Charge reversal of the negatively charged amino acid abolishes the nAChR-ethanol interaction. Moreover, using transgenic animals harboring the charge-reversal mutation, ex vivo measurements of muscle force production show that ethanol counters fatigue in wild type but not homozygous αE83K mutant animals. In accord, in vivo studies of motor coordination following ethanol administration reveal an approximately twofold improvement for wild type compared to homozygous mutant animals. Together, the converging results from molecular to animal studies suggest that ethanol counters muscle fatigue through its interaction with neuromuscular nAChRs.
Data from: Effects of nicotine on corneal wound healing following acute alkali burn
Epidemiological studies have indicated that smoking is a pivotal risk factor for the progression of several chronic diseases. Nicotine, the addictive component of cigarettes, has powerful pathophysiological properties in the body. Although the effects of cigarette smoking on corneal re-epithelialization have been studied, the effects of nicotine on corneal wound healing-related neovascularization and fibrosis have not been fully demonstrated. The aim of this study was to evaluate the effects of chronic administration of nicotine on corneal wound healing following acute insult induced by an alkali burn. BALB/C female mice randomly received either vehicle (2% saccharin) or nicotine (100 or 200 μg/ml in 2% saccharin) in drinking water ad libitum. After 1 week, animals were re-randomized and the experimental group was subjected to a corneal alkali burn, and then nicotine was administered until day 14 after the alkali burn. A corneal alkali burn model was generated by placing a piece of 2 mm-diameter filter paper soaked in 1N NaOH on the right eye. Histopathological analysis and the expression level of the pro-angiogenic genes vascular endothelial growth factor (VEGF) and matrix metalloproteinase-9 (MMP9) revealed that chronic nicotine administration enhanced alkali burn-induced corneal neovascularization. Furthermore, the mRNA expression of the pro-fibrogenic factors α-smooth muscle actin (αSMA), transforming growth factor-β (TGF-β), and collagen α1 (Col1) was enhanced in the high-concentration nicotine-treated group compared with the vehicle group after corneal injury. Immunohistochemical analysis also showed that the αSMA-positive area was increased in chronic nicotine-treated mice after corneal alkali burn. An in vitro assay found that expression of the α3, α7, and β1 nicotinic acetylcholine receptor (nAChR) subunits was significantly increased by chemical injury in human corneal fibroblast cells. Moreover, alkali-induced fibrogenic gene expression and proliferation of fibroblast cells were further increased by treatment with nicotine and cotinine. The proliferation of such cells induced by treatment of nicotine and cotinine was reduced by inhibition of the PI3K and PKC pathways using specific inhibitors. In conclusion, chronic administration of nicotine accelerated the angiogenic and fibrogenic healing processes in alkali-burned corneal tissue.
Varied effects of tobacco smoke and e-cigarette vapor suggest that nicotine does not affect endothelium-dependent relaxation and nitric oxide signaling
<p>Chronic smoking causes dysfunction of vascular endothelial cells, evident as a reduction of flow-mediated dilation in smokers, but the role of nicotine is still controversial. Given the increasing use of e-cigarettes and other nicotine products, it appears essential to clarify this issue. We studied extracts from cigarette smoke (CSE) and vapor from e-cigarettes (EVE) and heated tobacco (HTE) for their effects on vascular relaxation, endothelial nitric oxide signaling, and the activity of soluble guanylyl cyclase. The average nicotine concentrations of CSE, EVE, and HTE were 164, 800, and 85 µM, respectively. At a dilution of 1:3, CSE almost entirely inhibited the relaxation of rat aortas and porcine coronary arteries to acetylcholine and bradykinin, respectively, while undiluted EVE, with a 15-fold higher nicotine concentration, had no significant effect. With about 50% inhibition at 1:2 dilution, the effect of HTE was between CSE and EVE. Neither extract affected endothelium-independent relaxation to an NO donor. At the dilutions tested, CSE was not toxic to cultured endothelial cells but, in contrast to EVE, impaired NO signaling and inhibited NO stimulation of soluble guanylyl cyclase. Our results demonstrate that nicotine does not mediate the impaired endothelium-dependent vascular relaxation caused by smoking.</p>
The Effect of Nicotine Delivery Rate on Reinforcement
ClinicalTrials.gov study NCT03134339. IPD Sharing: NO. Countries: 1. Publications: 0.
Effects of Nicotine on Brain Opioid Receptors
ClinicalTrials.gov study NCT01040338. IPD Sharing: Not stated. Countries: 1. Publications: 0.
Developing Evidence to Inform Regulatory Policy on Nicotine Content in E-Liquids
ClinicalTrials.gov study NCT06619964. IPD Sharing: UNDECIDED. Countries: 1. Publications: 0.
Reduced Nicotine Cigarettes in Smokers With and Without Alcohol Use Disorder
ClinicalTrials.gov study NCT02990455. IPD Sharing: NO. Countries: 1. Publications: 0.
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Allen Brain Atlas
Allen Brain Atlas is an Allen Institute collection of brain map atlases, datasets, APIs, and analysis tools covering mouse, human, and non-human primate brain resources.
Annotated Behaviour and Observability Dataset (ABODe)
ABODe is a University of Edinburgh DataShare dataset for behavior classification in group-housed mice using home-cage video, identities, bounding boxes, ground-plate positions, and annotator labels.
DANDI Archive for NWB datasets
DANDI is a BRAIN Initiative archive for publishing and sharing neurophysiology data, including electrophysiology, optophysiology, and behavioral data packaged as NWB and related standards.
International Brain Laboratory public data
The International Brain Laboratory public data releases expose standardized mouse decision-making experiments, including Neuropixels recordings, widefield calcium imaging, behavior, and session metadata accessed through the ONE API.
OpenNeuro
OpenNeuro is a free, open platform for sharing neuroimaging datasets, with public search, dataset pages, and download paths for web, S3, DataLad, and the OpenNeuro CLI.