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Effect of D2 Antagonists in Smokers With Schizophrenia
Nicotine use in individuals with schizophrenia is extremely common, with recent estimates indicating that 80% of individuals with this condition smoke.[1] Greater smoking in this population has been linked to worse symptoms,[2] susceptibility to respiratory and cardiovascular diseases, and early mortality;[3] hence, reducing smoking in these patients is a key priority. Evidence suggests that patients taking first-generation antipsychotics, many of which produce potent dopamine (DA) D2 receptor antagonism, experience greater difficulty quitting with evidence-based cessation treatment.[4,5] Because these medications are foundational to the management of schizophrenia, an important question is whether DA D2 receptor antagonists modulate nicotine's reinforcing effects.
Want to quit smoking? Partner up: Couples who attempt to stop smoking together have a sixfold chance of success -- ScienceDaily
At the end of the programme, 64% of patients and 75% of partners were abstinent -- compared to none and 55% at the start, respectively. The odds of quitting smoking at 16 weeks were significantly higher (5.83-fold) in couples who tried to quit together compared to patients who attempted it alone.
"Previous research has shown that ex-smokers can also positively influence their spouse's attempts to quit, but in this study the effect was not statistically significant," said Ms Lampridou. "As for non-smoking partners, there is a strong risk that they will adopt their spouse's habit." Ms Lampridou noted that research is needed to confirm the findings in smokers who are otherwise healthy.
This is a neuron on nicotine: Nicotine works inside cells to reinforce addiction -- ScienceDaily
By making movies of cells containing biosensors in a lab dish, the team has discovered that nicotine enters into the endoplasmic reticulum within a few seconds of appearing outside a cell. Furthermore, the nicotine levels are more than enough to affect nAChRs during their assembly and to chaperone additional nAChRs on their journey to the cell surface. As a result, the neurons are more sensitive to the nicotine, which enhances the rewarding feelings after a puff on a tobacco cigarette or an e-cigarette. In other words, the more a person smokes, the more quickly and easily the smoker gets a nicotine buzz. This is part of nicotine addiction.
Dads' Nicotine Use May Cause Cognitive Problems for Children and Grandchildren - Neuroscience News
Analysis of spermatozoa from the original nicotine-exposed males indicated that promoter regions of multiple genes had been epigenetically modified, including the dopamine D2 gene, critical for brain development and learning, suggesting that these modifications likely contributed to the cognitive deficits in the descendants.
Differences between combined, isolated use of cannabis, nicotine on brain networks -- ScienceDaily
MRI scans were used to evaluate resting state functions in 12 different regions of the brain among four groups of participants: 28 nicotine users, 53 cannabis users, 26 nicotine and cannabis users, and 30 non-users in a control group. These scans revealed that the control group displayed greater connectivity in almost all of the networks compared to the nicotine and cannabis groups, while the combined nicotine plus cannabis group had greater connectivity than the only-nicotine and only-cannabis groups. Notably, this study did not demonstrate a correlation between substance use severity and functional connectivity.
Do children inherit drug protection from parents exposed to nicotine or drugs? Study suggests link between children and fathers -- ScienceDaily
What researchers found is that the offspring of nicotine-exposed fathers, compared to the offspring of fathers that were never exposed to nicotine, were protected from toxic levels of nicotine. Researchers then tested whether this resistance was specific for nicotine by treating both sets of offspring with cocaine, which acts via a wholly distinct molecular pathway than nicotine. Surprisingly, the children of nicotine-exposed fathers were also protected from cocaine. This multi-toxin resistance is likely a result of enhanced drug metabolism in the liver, and corresponds to an increase in expression levels of genes involved in drug metabolism. These genes were also packaged in a more open and accessible configuration in the liver cells, allowing for increased expression.
Do children inherit drug protection from parents exposed to nicotine or drugs? Study suggests link between children and fathers -- ScienceDaily
"Children born of fathers who have been exposed to nicotine are programmed to be not only more resistant to nicotine toxicity, but to other chemicals as well," said Dr. Rando, professor of biochemistry & molecular pharmacology. "If a similar phenomenon occurs in humans, this raises many important questions. For example, if your father smoked does that mean chemotherapy might be less effective for you? Are you more or less likely to smoke? It's important to understand what information is specifically being passed down from father to offspring and how that impacts us."
Nicotine withdrawal leads to reckless behavior?
The first period of nicotine abstinence proceeded as expected. The surprise came after three months when the lab rats suddenly became fearless and sought out well-lighted areas that prey animals normally avoid. At the same time, signaling in the brain's reward system changed, as shown by a study at Sahlgrenska Academy.
"This indicates very long-lasting changes caused by nicotine that were previously unknown. The nicotine appears to create a cascade of effects that only get worse and worse over time," says Julia Morud Lekholm, researcher in addiction biology at the Institute of Neuroscience and Physiology.
The experiment was done another two times. The researchers wanted to make sure that the unexpected results were not an isolated case. In total, 108 animals were tested, of which half received nicotine and half a salt solution over a three-week period. The outcome was the same every time.
"The nicotine treated animals spend much more time in these more frightening areas compared with those that only received salt solution injections. We don't see this right after the nicotine treatment, only after three or more months into abstinence. So then the animals have not received any nicotine for three months, and suddenly they demonstrate an increased spontaneous impulsiveness, which is very strange," says Julia Morud Lekholm.
Strong impact
"What's interesting is that at the same time we can also begin to see changes in the GABAergic system in the brain, which is the system that normally slows the brain's signaling," she continues.
After another four months, the GABA system in the studied region of the rats' brains was so strongly affected that it had been completely reversed. Instead of dampening the nerve cell signaling, it increased it.
In other words, a highly activated system, and an extensive risk of relapsing into smoking, for example, if people had been involved.
"Of course, rats and people are very different, but in terms of the type of brain circuit that we study, the brain's reward system, we are very much alike. Also in terms of risk-taking behavior, it's possible to translate to humans to some extent. Having poor impulse control isn't good for life in general, of course. One can end up in many bad situations and this may also have effects on the consumption of other drugs later in life," says Julia Morud Lekholm.