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Mark S. Gold - One of the best experts on this subject based on the ideXlab platform.
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Tobacco Smoke exposure induces nicotine dependence in rats
Psychopharmacology, 2010Co-Authors: Elysia Small, Hartmut Derendorf, Hina P. Shah, Jake J. Davenport, Jacqueline E. Geier, Kate R. Yavarovich, Hidetaka Yamada, Sreedharan N. Sabarinath, James R. Pauly, Mark S. GoldAbstract:Rationale Tobacco Smoke contains nicotine and many other compounds that act in concert on the brain reward system. Therefore, animal models are needed that allow the investigation of chronic exposure to the full spectrum of Tobacco Smoke constituents. Objectives The aim of these studies was to investigate if exposure to Tobacco Smoke leads to nicotine dependence in rats. Methods The intracranial self-stimulation procedure was used to assess the negative affective aspects of nicotine withdrawal. Somatic signs were recorded from a checklist of nicotine abstinence signs. Nicotine self-administration sessions were conducted to investigate if Tobacco Smoke exposure affects the motivation to self-administer nicotine. Nicotinic receptor autoradiography was used to investigate if exposure to Tobacco Smoke affects central α7 nicotinic acetylcholine receptor (nAChR) and non-α7 nAChR levels (primarily α4β2 nAChRs). Results The nAChR antagonist mecamylamine dose-dependently elevated the brain reward thresholds of the rats exposed to Tobacco Smoke and did not affect the brain reward thresholds of the untreated control rats. Furthermore, mecamylamine induced more somatic withdrawal signs in the Smoke-exposed rats than in the control rats. Nicotine self-administration was decreased 1 day after the last Tobacco Smoke exposure sessions and was returned to control levels 5 days later. Tobacco Smoke exposure increased the α7 nAChR density in the CA2/3 area and the stratum oriens and increased the non-α7 nAChR density in the dentate gyrus. Conclusion Tobacco Smoke exposure leads to nicotine dependence as indicated by precipitated affective and somatic withdrawal signs and induces an upregulation of nAChRs in the hippocampus.
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Tobacco Smoke exposure induces nicotine dependence in rats
Psychopharmacology, 2009Co-Authors: Elysia Small, Hartmut Derendorf, Hina P. Shah, Jacqueline E. Geier, Kate R. Yavarovich, Hidetaka Yamada, Sreedharan N. Sabarinath, James R. Pauly, Jake Davenport, Mark S. GoldAbstract:Rationale Tobacco Smoke contains nicotine and many other compounds that act in concert on the brain reward system. Therefore, animal models are needed that allow the investigation of chronic exposure to the full spectrum of Tobacco Smoke constituents.
Jonathan P. Winickoff - One of the best experts on this subject based on the ideXlab platform.
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Tobacco Smoke Incursions in Multiunit Housing
American journal of public health, 2014Co-Authors: Karen M. Wilson, Michelle Torok, Robert Mcmillen, Susanne E. Tanski, Jonathan D. Klein, Jonathan P. WinickoffAbstract:Objectives. We sought to describe the prevalence of secondhand Tobacco Smoke incursions reported by multiunit housing (MUH) residents, pinpoint factors associated with exposure, and determine whether Smoke-free building policy was associated with prevalence of reported Tobacco Smoke incursions.Methods. Data are from a 2011 nationally representative dual-frame survey (random-digit-dial and Internet panels) of US adults aged 18 years and older. Individuals who lived in MUH and who reported no smoking in their homes for the past 3 months, whether or not they reported being Smokers themselves, were included in this study. Incursions were defined as smelling Tobacco Smoke in their building or unit.Results. Of 562 respondents, 29.5% reported Smoke incursions in their buildings. Of these, 16% reported incursions in their own unit, 36.2% of which occurred at least weekly. Government-subsidized housing and partial Smoke-free policies were associated with a higher likelihood of reporting Smoke incursions.Conclusion...
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Acceptability of testing children for Tobacco-Smoke exposure: a national parent survey.
Pediatrics, 2011Co-Authors: Jonathan P. Winickoff, Robert Mcmillen, Susanne E. Tanski, Kaile M. Ross, Ellen A. Lipstein, Bethany Hipple, Joan Friebely, Jonathan D. KleinAbstract:WHAT THIS STUDY ADDS: This study shows that the majority of parents in general, and even parents who Smoke, want their children tested for Tobacco-Smoke exposure in the context of the child's health care setting. abstract Tests are available to measure children's exposure to Tobacco Smoke. One potential barrier to testing children for Tobacco- Smoke exposure is the belief that parents who Smoke would not want their child tested. No previous surveys have assessed whether testing children for exposure to Tobacco Smoke in the context of their child's primary care visit is acceptable to parents. OBJECTIVE: To assess whether testing children for Tobacco-Smoke ex- posure is acceptable to parents. DESIGN AND METHODS: We conducted a national random-digit-dial telephone survey of households from September to November 2006. The sample was weighted by race and gender, based on the 2005 US Census, to be representative of the US population. RESULTS: Of 2070 eligible respondents contacted, 1803 (87.1%) com- pleted the surveys. Among 477 parents in the sample, 60.1% thought that children should be tested for Tobacco-Smoke exposure at their child's doctor visit. Among the parental Smokers sampled, 62.0% thought that children should be tested for Tobacco-Smoke exposure at the child's doctor visit. In bivariate analysis, lower parental education level, allowing smoking in the home, nonwhite race, and female gender were each associated (P.05) with wanting the child tested for Tobacco-Smoke exposure. CONCLUSIONS: The majority of nonsmoking and smoking parents want their children tested for Tobacco-Smoke exposure during the child's health care visit. Pediatrics 2011;127:628-634
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Tobacco Smoke exposure in children who live in multiunit housing
Pediatrics, 2011Co-Authors: Karen M. Wilson, Jonathan D. Klein, Aaron K Blumkin, Mark Gottlieb, Jonathan P. WinickoffAbstract:There is no safe level of secondhand Tobacco-Smoke expo- sure, and no previous studies have explored multiunit housing as a potential contributor to secondhand Tobacco-Smoke exposure in chil- dren. We hypothesized that children who live in apartments have higher cotinine levels than those who live in detached homes, when controlling for demographics. METHODS: We analyzed data from the 2001-2006 National Health and Nu- trition Examination Survey. The housing types we included in our study were detached houses (including mobile homes), attached houses, and apartments. Our study subjects were children between the ages of 6 and 18 years. Cotinine levels were used to assess secondhand Tobacco-Smoke exposure, and those living with someone who Smoked inside the home were excluded. 2 tests, t tests, and Tobit regression models were used in Stata. Sample weights accounted for the complex survey design. RESULTS: Of 5002 children in our study, 73% were exposed to second- hand Tobacco Smoke. Children living in apartments had an increase in cotinine of 45% over those living in detached houses. This increase was 212% (P.01) for white residents and 46% (P.03) for black resi- dents, but there was no significant increase for those of other races/ ethnicities. At every cutoff level of cotinine, children in apartments had higher rates of exposure. The exposure effect of housing type was most pronounced at lower levels of cotinine. CONCLUSIONS: Most children without known secondhand Tobacco- Smoke exposure inside the home still showed evidence of Tobacco-Smoke exposure. Children in apartments had higher mean cotinine levels than children in detached houses. Potential causes for this result could be seepage through walls or shared ventilation systems. Smoking bans in multiunit housing may reduce children's exposure to Tobacco Smoke. Pediatrics 2011;127:85-92
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Tobacco Smoke exposure and chronic conditions of childhood.
Pediatrics, 2010Co-Authors: Jonathan P. Winickoff, Jeanne Van Cleave, Nicolas M. OreskovicAbstract:Two remarkable articles by Kwok et al1 and Brion et al2 in this month's Pediatrics tighten the evidence around Tobacco Smoke exposure and chronic conditions of childhood. Their work adds to previous research findings that demonstrated associations between Tobacco Smoke exposure and various childhood morbidities and mortality (Table 1).3 Indeed, 3 important categories of chronic conditions of childhood (asthma, obesity, and mental health disorders) have small-to-moderate independent associations with Tobacco Smoke exposure either during pregnancy or in the postnatal period. Dental caries are one of the most common chronic conditions of childhood, and a moderate independent association with Tobacco Smoke exposure has been described.4 View this table: TABLE 1 Specific Health Effects of Prenatal and Postnatal Exposure to Tobacco Smoke Following a large Hong Kong birth cohort, Kwok et al1 found an association between Tobacco Smoke exposure of pregnant mothers and subsequent child overweight. The study is methodologically important, because it examined this effect among mothers who themselves did not Smoke but were exposed by the father. That … Address correspondence to Jonathan P. Winickoff, MD, MPH, Center for Child and Adolescent Health Policy, Massachusetts General Hospital for Children, 50 Staniford St, Suite 901, Boston, MA 02114. E-mail: jwinickoff{at}partners.org
Hartmut Derendorf - One of the best experts on this subject based on the ideXlab platform.
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Tobacco Smoke exposure enhances reward sensitivity in male and female rats
Psychopharmacology, 2021Co-Authors: Ranjithkumar Chellian, Isaac Wilks, Brandon Levin, Song Xue, Azin Behnood-rod, Ryann Wilson, Megan Mccarthy, Abhigyan Ravula, Hardik Chandasana, Hartmut DerendorfAbstract:Rationale Systemic administration of the Tobacco Smoke constituent nicotine stimulates brain reward function in rats. However, it is unknown if the inhalation of Tobacco Smoke affects brain reward function. Objectives These experiments investigated if exposure to Smoke from high-nicotine SPECTRUM research cigarettes increases reward function and affects the rewarding effects of nicotine in adult male and female Wistar rats. Methods Reward function after Smoke or nicotine exposure was investigated using the intracranial self-stimulation (ICSS) procedure. A decrease in reward thresholds reflects an increase in reward function. In the first experiment, the rats were exposed to Tobacco Smoke for 40 min/day for 9 days, and the rewarding effects of nicotine (0.03–0.6 mg/kg) were investigated 3 weeks later. In the second experiment, the dose effects of Tobacco Smoke exposure (40-min sessions, 1–4 cigarettes burnt simultaneously) on reward function were investigated. Results Tobacco Smoke exposure did not affect the nicotine-induced decrease in reward thresholds or response latencies in male and female rats. Smoke exposure lowered the brain reward thresholds to a similar degree in males and females and caused a greater decrease in latencies in females. There was a positive relationship between plasma nicotine and cotinine levels and the nicotine content of the SPECTRUM research cigarettes. Similar Smoke exposure conditions led to higher plasma nicotine and cotinine levels in female than male rats. Conclusion These findings indicate that Tobacco Smoke exposure enhances brain reward function but does not potentiate the rewarding effects of nicotine in male and female rats.
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Repeated pre-exposure to Tobacco Smoke potentiates subsequent locomotor responses to nicotine and Tobacco Smoke but not amphetamine in adult rats.
Pharmacology biochemistry and behavior, 2011Co-Authors: Adrie W. Bruijnzeel, Gene Rodrick, Rajendra P. Singh, Hartmut Derendorf, Rayna M. BauzoAbstract:Abstract These studies investigated if pre-exposure to Tobacco Smoke affects the locomotor response to Tobacco Smoke, nicotine, and amphetamine in adult rats. The rats were habituated to an open field for 3–4 days and then exposed to Tobacco Smoke for 2 h/day for 13–14 days. The effect of exposure to Tobacco Smoke on locomotor activity was investigated after 1, 7, and 14 days of Smoke exposure and after one 2-hour exposure session that followed a 3-week off period. The effects of Tobacco Smoke on the locomotor responses to nicotine (0.04 and 0.4 mg/kg, base) and amphetamine (0.1 and 0.5 mg/kg) were investigated on day 14, one day after the last Smoke exposure session. The locomotor response to Tobacco Smoke was increased after 7 and 14 days of Smoke exposure and after one exposure session after the 3-week off-period. The acute administration of the high dose of nicotine (0.4 mg/kg) led to a brief period of hypoactivity that was followed by a period of hyperactivity. Pre-exposure to Tobacco Smoke attenuated the nicotine-induced hypoactivity and potentiated the nicotine-induced hyperactivity. The low dose of nicotine (0.04 mg/kg) did not affect locomotor activity in the control rats but increased the total distance traveled in the Tobacco Smoke exposed rats. Exposure to Tobacco Smoke did not affect the locomotor response to amphetamine. These findings indicate that exposure to Tobacco Smoke leads to tolerance to the depressant effects of nicotine and potentiates the stimulant effects of nicotine and Tobacco Smoke.
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Tobacco Smoke exposure induces nicotine dependence in rats
Psychopharmacology, 2010Co-Authors: Elysia Small, Hartmut Derendorf, Hina P. Shah, Jake J. Davenport, Jacqueline E. Geier, Kate R. Yavarovich, Hidetaka Yamada, Sreedharan N. Sabarinath, James R. Pauly, Mark S. GoldAbstract:Rationale Tobacco Smoke contains nicotine and many other compounds that act in concert on the brain reward system. Therefore, animal models are needed that allow the investigation of chronic exposure to the full spectrum of Tobacco Smoke constituents. Objectives The aim of these studies was to investigate if exposure to Tobacco Smoke leads to nicotine dependence in rats. Methods The intracranial self-stimulation procedure was used to assess the negative affective aspects of nicotine withdrawal. Somatic signs were recorded from a checklist of nicotine abstinence signs. Nicotine self-administration sessions were conducted to investigate if Tobacco Smoke exposure affects the motivation to self-administer nicotine. Nicotinic receptor autoradiography was used to investigate if exposure to Tobacco Smoke affects central α7 nicotinic acetylcholine receptor (nAChR) and non-α7 nAChR levels (primarily α4β2 nAChRs). Results The nAChR antagonist mecamylamine dose-dependently elevated the brain reward thresholds of the rats exposed to Tobacco Smoke and did not affect the brain reward thresholds of the untreated control rats. Furthermore, mecamylamine induced more somatic withdrawal signs in the Smoke-exposed rats than in the control rats. Nicotine self-administration was decreased 1 day after the last Tobacco Smoke exposure sessions and was returned to control levels 5 days later. Tobacco Smoke exposure increased the α7 nAChR density in the CA2/3 area and the stratum oriens and increased the non-α7 nAChR density in the dentate gyrus. Conclusion Tobacco Smoke exposure leads to nicotine dependence as indicated by precipitated affective and somatic withdrawal signs and induces an upregulation of nAChRs in the hippocampus.
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Tobacco Smoke exposure induces nicotine dependence in rats
Psychopharmacology, 2009Co-Authors: Elysia Small, Hartmut Derendorf, Hina P. Shah, Jacqueline E. Geier, Kate R. Yavarovich, Hidetaka Yamada, Sreedharan N. Sabarinath, James R. Pauly, Jake Davenport, Mark S. GoldAbstract:Rationale Tobacco Smoke contains nicotine and many other compounds that act in concert on the brain reward system. Therefore, animal models are needed that allow the investigation of chronic exposure to the full spectrum of Tobacco Smoke constituents.
Akimichi Morita - One of the best experts on this subject based on the ideXlab platform.
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Tobacco Smoke induced skin pigmentation is mediated by the aryl hydrocarbon receptor
Experimental Dermatology, 2013Co-Authors: Motoki Nakamura, Yukiko Ueda, Mai Hayashi, Hiroshi Kato, Takuya Furuhashi, Akimichi MoritaAbstract:It is widely recognized that Tobacco Smoke causes skin pigmentation. No studies, however, have directly evaluated the mechanisms of the changes in Smoker's skin pigmentation. In this study, when cultured with water-soluble Tobacco Smoke extract, the human epidermal melanocytes grew to a large size and produced more melanins. We evaluated melanocyte activation by quantifying microphthalmia-associated transcription factor (MITF) expression by real-time polymerase chain reaction. MITF expression was significantly and dose-dependently increased by exposure to Tobacco Smoke extract. The Wnt/β-catenin signalling pathway seemed to mediate the Tobacco Smoke extract-induced melanocyte activation. Immunocytochemical studies revealed that the activated melanocytes actively expressed aryl hydrocarbon receptors (AhR) around the nuclear membrane. The Tobacco Smoke extract-induced MITF activation was inhibited by RNA silencing of the AhR. This study provides the evidence that Tobacco Smoke enhances pigmentation in vitro and that the increase in pigmentation may involve β-catenin- and AhR-mediated mechanisms inside human melanocytes.
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Molecular basis of Tobacco Smoke-induced premature skin aging.
The journal of investigative dermatology. Symposium proceedings, 2009Co-Authors: Akimichi Morita, Kan Torii, Akira Maeda, Yuji YamaguchiAbstract:Although it is now widely recognized that Tobacco Smoke has negative effects on the skin, the molecular mechanisms underlying its skin-aging effects remain uncertain. Epidemiological studies indicate that Tobacco smoking is a strong independent predictor of facial wrinkle formation and other aspects of premature skin aging. Recent in vivo studies in humans and mice provided the first direct evidence that Tobacco Smoke causes premature skin aging, and they have begun to reveal the molecular changes in the skin that occur in response to it. Water-soluble Tobacco Smoke extract, which predominantly produces oxidative stress when applied topically to cultured skin fibroblasts, impairs collagen biosynthesis. Matrix metalloproteinases, which degrade collagen, are induced dose-dependently by Tobacco Smoke extract as well as by other constituents that trigger the aryl hydrocarbon receptor (AhR), a ligand-dependent transcription factor that mediates the toxicity of several environmental contaminants, including photoproducts in the body generated by UVB radiation. Tobacco Smoke also contains many non-water-soluble constituents that activate the AhR pathway. Our most recent studies using hexane-soluble Tobacco extract indicate that activation of the AhR pathway may play a role in the premature skin-aging effects of Tobacco Smoke exposure.
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Tobacco Smoke causes premature skin aging
Journal of Dermatological Science, 2007Co-Authors: Akimichi MoritaAbstract:Smoking Tobacco is the most preventable cause of morbidity and is responsible for more than three million deaths a year worldwide. In addition to a strong association with a number of systemic diseases, smoking is also associated with many dermatological conditions, including poor wound healing, premature skin aging, squamous cell carcinoma, melanoma, oral cancer, acne, psoriasis, and hair loss. This review focuses on the effects of smoking on premature skin aging. It has been long established that smoking has deleterious effects on skin. Epidemiological studies indicate that smoking is an important environmental factor in premature skin aging. In vitro studies indicate that Tobacco Smoke extract impairs the production of collagen and increases the production of tropoelastin and matrix metalloproteinases (MMP), which degrade matrix proteins, and also causes an abnormal production of elastosis material. Smoking increases MMP levels, which leads to the degradation of collagen, elastic fibers, and proteoglycans, suggesting an imbalance between biosynthesis and degradation in dermal connective tissue metabolism. Reactive oxygen species are also involved in Tobacco Smoke-induced premature skin aging. Scavengers of reactive oxygen species ameliorate the induction of MMP. Tobacco Smoke extract also impacts dermal connective tissue in nude mice. Thus, in vitro and in vivo evidence indicates that smoking Tobacco leads to accelerated aging of the skin. These findings might be useful to motivate those patients who are more concerned about their appearance than the potential internal damage associated with smoking to stop smoking.
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Tobacco Smoke and Skin Aging
Cigarette Smoke and Oxidative Stress, 1Co-Authors: Akimichi MoritaAbstract:15.2 Molecular Mechanisms of Tobacco Smoke-Induced Skin Aging . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 380 15.2.1 Effects of Tobacco Smoke on Skin Models In Vitro 381 15.2.3 Effect of Tobacco Smoke In Vivo . . . . . . . . . . . . . . . . 381 15.3. Some Molecular Mechanisms and Protective Factors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 382 15.4. Conclusions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 383 References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 383
Elysia Small - One of the best experts on this subject based on the ideXlab platform.
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Tobacco Smoke exposure induces nicotine dependence in rats
Psychopharmacology, 2010Co-Authors: Elysia Small, Hartmut Derendorf, Hina P. Shah, Jake J. Davenport, Jacqueline E. Geier, Kate R. Yavarovich, Hidetaka Yamada, Sreedharan N. Sabarinath, James R. Pauly, Mark S. GoldAbstract:Rationale Tobacco Smoke contains nicotine and many other compounds that act in concert on the brain reward system. Therefore, animal models are needed that allow the investigation of chronic exposure to the full spectrum of Tobacco Smoke constituents. Objectives The aim of these studies was to investigate if exposure to Tobacco Smoke leads to nicotine dependence in rats. Methods The intracranial self-stimulation procedure was used to assess the negative affective aspects of nicotine withdrawal. Somatic signs were recorded from a checklist of nicotine abstinence signs. Nicotine self-administration sessions were conducted to investigate if Tobacco Smoke exposure affects the motivation to self-administer nicotine. Nicotinic receptor autoradiography was used to investigate if exposure to Tobacco Smoke affects central α7 nicotinic acetylcholine receptor (nAChR) and non-α7 nAChR levels (primarily α4β2 nAChRs). Results The nAChR antagonist mecamylamine dose-dependently elevated the brain reward thresholds of the rats exposed to Tobacco Smoke and did not affect the brain reward thresholds of the untreated control rats. Furthermore, mecamylamine induced more somatic withdrawal signs in the Smoke-exposed rats than in the control rats. Nicotine self-administration was decreased 1 day after the last Tobacco Smoke exposure sessions and was returned to control levels 5 days later. Tobacco Smoke exposure increased the α7 nAChR density in the CA2/3 area and the stratum oriens and increased the non-α7 nAChR density in the dentate gyrus. Conclusion Tobacco Smoke exposure leads to nicotine dependence as indicated by precipitated affective and somatic withdrawal signs and induces an upregulation of nAChRs in the hippocampus.
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Tobacco Smoke exposure induces nicotine dependence in rats
Psychopharmacology, 2009Co-Authors: Elysia Small, Hartmut Derendorf, Hina P. Shah, Jacqueline E. Geier, Kate R. Yavarovich, Hidetaka Yamada, Sreedharan N. Sabarinath, James R. Pauly, Jake Davenport, Mark S. GoldAbstract:Rationale Tobacco Smoke contains nicotine and many other compounds that act in concert on the brain reward system. Therefore, animal models are needed that allow the investigation of chronic exposure to the full spectrum of Tobacco Smoke constituents.
