Displaying publications 41 - 60 of 69 in total

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  1. Picco L, Subramaniam M, Abdin E, Vaingankar JA, Chong SA
    Ann Acad Med Singap, 2012 Aug;41(8):325-34.
    PMID: 23010809
    INTRODUCTION: Smoking is one of the leading preventable causes of death throughout the world and can lead to nicotine dependence, particularly when initiated at a young age. This paper describes the prevalence of smoking and nicotine dependence in the adult Singapore resident population, whilst also exploring rates among the major ethnic groups (Chinese, Malay and Indian), different education levels and those with chronic psychiatric and physical comorbidities.

    MATERIAL AND METHODS: The Singapore Mental Health Study (SMHS) is a cross-sectional epidemiological study that was conducted between December 2009 and December 2010. Information on smoking status was assessed using the Composite International Diagnostic Interview version 3.0 (CIDI 3.0) and the Fagerstrom Test for Nicotine Dependence measured nicotine dependence. Socio-demographic information was also collected.

    RESULTS: In total, 6616 respondents participated in the SMHS giving a response rate of 75.9%. We found that 16% of the population were current smokers and 4.5% had nicotine dependence. Current smokers were more likely to be younger (18 to 34 years old), males, Malay and have lower education, whilst males had a 4.6 times higher risk of nicotine dependence to that of females. The prevalence of nicotine dependence was also higher in those with alcohol abuse and those experiencing chronic pain.

    CONCLUSION: The results from this study highlight the important differences in the prevalence of smoking and nicotine dependence among different age groups, gender and ethnicity in Singapore and are important for developing future health policies and targeted preventive strategies.

    Matched MeSH terms: Nicotine*
  2. Abd Rashid N, Hapidin H, Abdullah H, Ismail Z, Long I
    Brain Behav, 2017 06;7(6):e00704.
    PMID: 28638710 DOI: 10.1002/brb3.704
    INTRODUCTION: REM sleep deprivation is associated with impairment in learning and memory, and nicotine treatment has been shown to attenuate this effect. Recent studies have demonstrated the importance of DREAM protein in learning and memory processes. This study investigates the association of DREAM protein in REM sleep-deprived rats hippocampus upon nicotine treatment.

    METHODS: Male Sprague Dawley rats were subjected to normal condition, REM sleep deprivation and control wide platform condition for 72 hr. During this procedure, saline or nicotine (1 mg/kg) was given subcutaneously twice a day. Then, Morris water maze (MWM) test was used to assess learning and memory performance of the rats. The rats were sacrificed and the brain was harvested for immunohistochemistry and Western blot analysis.

    RESULTS: MWM test found that REM sleep deprivation significantly impaired learning and memory performance without defect in locomotor function associated with a significant increase in hippocampus DREAM protein expression in CA1, CA2, CA3, and DG regions and the mean relative level of DREAM protein compared to other experimental groups. Treatment with acute nicotine significantly prevented these effects and decreased expression of DREAM protein in all the hippocampus regions but only slightly reduce the mean relative level of DREAM protein.

    CONCLUSION: This study suggests that changes in DREAM protein expression in CA1, CA2, CA3, and DG regions of rat's hippocampus and mean relative level of DREAM protein may involve in the mechanism of nicotine treatment-prevented REM sleep deprivation-induced learning and memory impairment in rats.

    Matched MeSH terms: Nicotine/pharmacology*
  3. Bisong SA, Ukoh IE, Nna VU, Ebong PE
    Andrologia, 2018 Sep;50(7):e13050.
    PMID: 29806220 DOI: 10.1111/and.13050
    Previous studies showed that exposure to stress or nicotine induced reproductive impairment in male rats. Here, we assessed the effect of an antioxidant (vitamin E) on nicotine-, stress- and nicotine + stress-induced reproductive impairment in male rats. Forty-eight male albino Wistar rats were divided into eight groups as follows; control, stress (generator noise 90-120 dB, 8 hr/day), nicotine (1.5 mg kg-1 day-1 ), nicotine + stress, vitamin E (100 mg kg-1 day-1 ), stress + vitamin E, nicotine + vitamin E and stress + nicotine + vitamin E. Sperm count, viability, motility and rapid progressive forward movement decreased significantly (p 
    Matched MeSH terms: Nicotine/toxicity
  4. Chellian R, Pandy V
    Biomed Pharmacother, 2018 Dec;108:1591-1595.
    PMID: 30372861 DOI: 10.1016/j.biopha.2018.09.137
    Alpha-asarone is one of the bioactive phytochemicals present in the rhizomes of Acorus species and demonstrated its anticonvulsant activity in rodents. Alpha-asarone protected mice from the gamma-aminobutyric acid (GABA) type A receptor antagonist or N-methyl-d-aspartate (NMDA) receptor agonist-induced seizures. In our recent study, α-asarone attenuated the nicotine withdrawal-induced depression-like behavior in mice. The seizures induced by nicotine is mediated through the activation of nicotinic acetylcholine receptors (nAChRs) and stimulation of NMDA receptors. Therefore, we hypothesized that α-asarone might be effective against nicotine-induced seizures. Also, the interaction of α-asarone with nAChRs is unknown. In this study, we investigated the effect of α-asarone on the locomotor activity and body temperature in mice. In addition, we studied the effect of α-asarone on nicotine-induced seizures in mice. Finally, we assessed in vivo pharmacodynamic interaction of α-asarone with nAChRs using nicotine-induced hypomotility and hypothermia tests in mice. The results of this study showed that the α-asarone (50-200 mg/kg, i.p.) and diazepam (5 mg/kg, i.p.) treatment significantly decreased the locomotor activity and body temperature in mice. Furthermore, α-asarone (50-200 mg/kg, i.p.) and diazepam (5 mg/kg, i.p.) pretreatment significantly prolonged the onset time of nicotine-induced seizures in mice. However, α-asarone (30 and 50 mg/kg, i.p.) pretreatment did not inhibit the nicotine-induced hypomotility or hypothermia in mice. Conversely, mecamylamine (1 mg/kg, s.c.) pretreatment completely blocked the nicotine-induced seizures and significantly prevents the nicotine-induced hypomotility and hypothermia in mice. Overall, these results suggest that the protective effect of α-asarone against nicotine-induced seizures did not mediate through the antagonism of nAChRs. We also postulated that the GABAergic and glutamatergic activities of α-asarone could be involved in its protective effect against nicotine-induced seizures and based on this aspect further studies are required.
    Matched MeSH terms: Nicotine/toxicity*
  5. Norazlina M, Lee PL, Lukman HI, Nazrun AS, Ima-Nirwana S
    Singapore Med J, 2007 Mar;48(3):195-9.
    PMID: 17342286
    Nicotine has been shown to exert negative effects on bone. This study determined whether vitamin E supplementation is able to repair the nicotine-induced adverse effects in bone.
    Matched MeSH terms: Nicotine/pharmacology*
  6. Kamsani YS, Rajikin MH, Mohamed Nor Khan NA, Abdul Satar N, Chatterjee A
    Med Sci Monit Basic Res, 2013 Mar 06;19:87-92.
    PMID: 23462735 DOI: 10.12659/MSMBR.883822
    BACKGROUND: This study aimed to evaluate the adverse effects of various doses of nicotine and protective effects of different concentrations of gamma-tocotrienol (gamma-TCT) on in vitro embryonic development and lipid peroxidation in mice.

    MATERIAL AND METHODS: A) Effects of various doses of nicotine on in vitro embryonic development: Female mice were treated with 1.0, 3.0, or 5.0 mg/kg/day nicotine for 7 consecutive days. Animals were superovulated, cohabited overnight, and sacrificed. Embryos were cultured in vitro. Plasma was assayed. B) Effects of concomitant treatment of nicotine concurrently with various doses of gamma-TCT on in vitro embryonic development: Female mice were treated with nicotine (5.0 mg/kg/day), gavaged gamma-TCT of 30, 60, or 90 mg/kg/day or nicotine concurrently with gamma-TCT of 3 different doses for 7 consecutive days. Animals were superovulated, cohabited overnight, and sacrificed. Embryos were cultured and plasma was assayed.

    RESULTS: A) Effects of various doses of nicotine on in vitro embryonic development: Number of hatched blastocysts decreased in 1.0 and 3.0 mg/kg/day nicotine groups. Nicotine at 5.0 mg/kg/day stopped embryo development at morula. MDA concentrations increased following all nicotine doses. B) Effects of concomitant treatment of nicotine concurrently with various doses of gamma-TCT on in vitro embryonic development: Embryo development was completed in all groups. MDA concentration increased only in the group treated with nicotine concurrently with 30 mg/kg/day gamma-TCT.

    CONCLUSIONS: Nicotine impairs in vitro embryo development and increases MDA in plasma. The deleterious impact of nicotine on embryo development is reversed by supplementing gamma-TCT concurrently with nicotine.

    Matched MeSH terms: Nicotine/pharmacology
  7. He L, Gong H, Zhang J, Zhong C, Huang Y, Zhang C, et al.
    Saudi J Biol Sci, 2016 Jul;23(4):531-41.
    PMID: 27298588 DOI: 10.1016/j.sjbs.2016.02.021
    The effects of differences in smoke concentration and exposure duration in Sprague Dawley rats to determine variation in type and severity of the testis apoptosis were evaluated. The daily dosages were 10, 20 and 30 non-filter cigarettes for a period of 2, 4, 6, 8 and 12 weeks. Mainstream smoke exposure suppressed body weight gain in all regimens. A dose-related increase in plasma nicotine concentration was observed in smoke-exposed groups for 4, 6, 8 and 12 week regimens. Histopathological examination of the exposed groups showed disturbances in the stages of spermatogenesis, tubules atrophying and these appeared to be dose-related. Cytoplasmic caspase-3 immunostaining was detected both in Sertoli cells and germ cells in smoke-exposure groups. An increase in TUNEL-positive cells of testicular cells was observed after 6 weeks of cigarette exposure. The results indicate that cigarette exposure concentration and duration have interaction effect to induce apoptosis in the rat testes.
    Matched MeSH terms: Nicotine
  8. Sanip Z, Hanaffi SH, Ahmad I, Yusoff SS, Rasool AH, Yusoff HM
    Tob Induc Dis, 2015;13(1):32.
    PMID: 26346914 DOI: 10.1186/s12971-015-0052-9
    BACKGROUND: Studies have demonstrated that secondhand smoke (SHS) exposure could impair endothelial function. However, the effect of SHS exposure specifically on microvascular endothelial function is not well understood. This study aimed to determine the effects of SHS exposure on microvascular endothelial function among non-smoking, generally healthy women.

    FINDINGS: We studied 127 women; and based on their hair nicotine levels measured using gas chromatography-mass spectrometry, 25 of them were categorized as having higher hair nicotine levels, 25 were grouped as having lower hair nicotine and 77 women were grouped into the non-detected group. The non-detected group did not have detectable levels of hair nicotine. Anthropometry, blood pressure (BP), lipid profile and high-sensitivity C-reactive protein (hsCRP) were measured accordingly. Microvascular endothelial function was assessed non-invasively using laser Doppler fluximetry and the process of iontophoresis involving acetylcholine and sodium nitroprusside as endothelium-dependent and endothelium-independent vasodilators respectively. The mean hair nicotine levels for higher and lower hair nicotine groups were 0.74 (1.04) and 0.05 (0.01) ng/mg respectively. There were no significant differences in anthropometry, BP, lipid profile and hsCRP between these groups. There were also no significant differences in the microvascular perfusion and endothelial function between these groups.

    CONCLUSION: In this study, generally healthy non-smoking women who have higher, lower and non-detected hair nicotine levels did not show significant differences in their microvascular endothelial function. Low levels of SHS exposure among generally healthy non-smoking women may not significantly impair their microvascular endothelial function.

    Matched MeSH terms: Nicotine
  9. Singh R, Bansal Y, Parhar I, Kuhad A, Soga T
    Neurochem Int, 2019 12;131:104545.
    PMID: 31494132 DOI: 10.1016/j.neuint.2019.104545
    Neuropsychiatric disorders (NPDs) exert a devastating impact on an individual's personal and social well-being, encompassing various conditions and brain anomalies that influence affect, cognition, and behavior. Because the pathophysiology of NPDs is multifactorial, the precise mechanisms underlying the development of such disorders remain unclear, representing a unique challenge in current neuropsychopharmacotherapy. Transient receptor potential vanilloid (TRPV) type channels are a family of ligand-gated ion channels that mainly include sensory receptors that respond to thermal, mechanical and chemical stimuli. TRPV channels are abundantly present in dopaminergic neurons, thus playing a pivotal role in the modulation of the reward system and in pathophysiology of diseases such as stress, anxiety, depression, schizophrenia, neurodegenerative disorders and substance abuse/addiction. Recent evidence has highlighted TRPV channels as potential targets for understanding modulation of the reward system and various forms of addiction (opioids, cocaine, amphetamines, alcohol, nicotine, cannabis). In this review, we discuss the distribution, physiological roles, ligands and therapeutic importance of TRPV channels with regard to NPDs and addiction biology.
    Matched MeSH terms: Nicotine
  10. Draman S, Ab Rahman NS, Nik Mohamed MH, Ab Rahman J, Kartiwi M
    J Pharm Bioallied Sci, 2020 Nov;12(Suppl 2):S718-S727.
    PMID: 33828367 DOI: 10.4103/jpbs.JPBS_384_19
    Context: Electronic cigarettes have been used as a harm reduction method toward tobacco cessation. Malaysian government has enforced a strict policy to regulate the sale of electronic cigarette products because its liquid contains nicotine.

    Aims: This study aimed to explore the general public's perception toward electronic cigarette use. Public support toward electronic cigarette regulation was also examined.

    Settings and Design: This was a Malaysian population-based survey.

    Materials and Methods: Data were obtained from the National E-Cigarette Survey (NECS) 2016, which used a multistage stratified cluster sampling household survey representing all Malaysian adults aged 18 years old. A cross-sectional survey was conducted among a total of 4288 adults.

    Statistical Analysis Used: Descriptive and logistic regression analysis.

    Results: Majority were aged 25-44 years old (44%), completed at least secondary education (69%), of Malay ethnicity (73%), and married (68%). Majority (88.1%) have never used electronic cigarette. A quarter (25.5%) perceived electronic cigarette helps people quit cigarette smoking, whereas 20.3% perceived electronic cigarette helps people to maintain cigarette abstinence. Approximately 85% believed that electronic cigarette use does not help in improving breathing and coughing. Majority (91.8%) disagreed that electronic cigarettes should be allowed in places where tobacco smoking is banned. Thus, 63.4% agreed that electronic cigarette should be banned completely rather than regulated.

    Conclusion: Majority of general public had negative perception about electronic cigarette use.

    Matched MeSH terms: Nicotine
  11. Herlambang Devianto, Desiana Radithia, Bagus Soebadi, Adiastuti Endah Parmadiati, Rosnah Zain
    MyJurnal
    Introduction: One of the risk factors for cancer is the habit of smoking. Some carcinogenic substances in ciga-rettes are nicotine and nitrosamine. In cigarette smoke there are free radical molecules or Reactive Oxygen Species (ROS) that can cause DNA mutations that can disrupt the balance of cell metabolism. One of them is the apoptosis, apoptosis is a programmed cell death mechanism. In cancer conditions there are apoptotic disorders and excessive proliferation of cells. The process of apoptosis is influenced by the death receptor, Tumor Necrosis Factor apoptosis inducing ligand R1 (TRAIL R1). This study aims to determine the effect of smoke exposure to expression of TRAIL R1 on the mucosal epithelium of the tongue of the Wistar rat (Rattus Novergicus). Methods: The subjects of this study were 24 male Rattus Novergicus with the age range of 12-14 weeks and weighing ± 170 grams. Divided into 4 groups with 2 control groups 4 weeks (K4), 8 weeks (K8) and 2 treatment groups each given 2 cigarettes / day ex-posure to cigarette smoke for each rat for 4 weeks (P4) and 8 weeks (P8). Results: The results showed that exposure to cigarette smoke can cause interference with TRAIL R1 expression. There was a significant difference in TRAIL R1 expression between the control and treatment groups and there was a significant difference in TRAIL R1 expression between the duration of cigarette smoke exposure (P4 and P8). Conclusion: Exposure to cigarette smoke can interfere with the process of apoptosis.
    Matched MeSH terms: Nicotine
  12. Zulkifli MH, Viswenaden P, Jasamai M, Azmi N, Yaakob NS
    Biomed Pharmacother, 2019 Feb 20;112:108630.
    PMID: 30797147 DOI: 10.1016/j.biopha.2019.108630
    5-HT3R antagonists such as ondansetron, granisetron and tropisetron have been clinically used to treat nausea and vomiting in chemotherapy patients. However, current study and research revealed novel potentials of these ligands in other diseases like inflammation, Alzheimer's, and drug abuse. Towards utilising these drugs as anti-smoking agents to treat nicotine dependence problem, there are conflicting reports regarding the potential of these ligands in modulating the effects of nicotine in both human and animal behavioural studies. This is complicated by the heterogeneity of 5-HT3R itself, cross regulation between nicotinic acetylcholinergic receptor (nAChR) and distinct pharmacological profiles of 5-HT3R antagonists. This review gathered existing studies conducted investigating the potential of "-setron" class of 5-HT3R antagonists in modulating nicotine effects. We proposed that the mechanism where 5-HT3R antagonists mediate the effects of nicotine could be attributed by both direct at 5-HT3R and indirect mechanism in nicotine addiction downstream regulation. The indirect mechanism mediated by the 5-HT3R antagonist could be through α7 nAChR, 5-HT1B receptor (5-HT1BR), 5-HT1C receptor (5-HT1CR), calcineurin activity, p38 MAPK level, PPAR-γ and NF-κβ. Our review suggested that future studies should focus on newer 5-HT3R antagonist with superior pharmacological profile or the one with multitarget action rather than high selectivity at single receptor.
    Matched MeSH terms: Nicotine
  13. Yuhaniza Shafinie Kamsani, Mohd Hamim Rajikin
    This review summarizes the impact of tocotrienols (TCTs) as antioxidants in minimizing
    oxidative stress (OS), particularly in embryos exposed to OS causing agents. OS level is
    increased, for example, by nicotine, a major alkaloid content in cigarette, which is also a source
    of exogenous reactive oxygen species (ROS). Increased nicotine-induced OS increases cell
    stress response, which is a common trigger leading to embryonic cell death. Having more
    profound anti-oxidative stress effects than its counterpart tocopherol, TCTs improve blastocyst
    implantation, foetal growth, pregnancy outcome and survival of the neonates affected by
    nicotine. In reversing cell developmental arrest caused by nicotine-induced OS, TCTs enhances
    PDK-1 expression in the P13K/Akt pathway and permit embryonic development beyond the 4-
    cell stage with the production of more morulae. At the cytoskeletal level, TCTs increase the
    number of nicotine-induced apoptotic cells, through caspase 8 activation in the mitochondria.
    TCTs facilitate rough endoplasmic reticulum (rER) stress-mediated apoptosis and autophagy,
    resulting from nicotine-induced OS. Reduced vesicular population in TCT supplemented
    oocytes on the other hand may suggest reduced secretion of apoptotic cell bodies thus probably
    minimizing vesicular apoptosis during oocyte maturation. Further extensive research is
    required to develop TCTs as a tool in specific therapeutic approaches to overcome the
    detrimental effects of OS.
    Matched MeSH terms: Nicotine
  14. Md Mizanur Rahman, Mohd Taha Arif, Mohd Fadzillah Abd Razak, Mohd Raili bin Suhaili, Zainab Tambi, Akoi, Cliffton, et al.
    MyJurnal
    Menthol brand cigarette has been found to be linked with early initiation of smoking and addiction of nicotine. This study was designed to find out the factors associated with smoking menthol brand cigarettes among adult population in Sarawak. This was a cross-sectional study conducted among the adult population in Sarawak. Data were collected from ten villages in Kota Samarahan and Kuching Division by face to face interview using modified Global Adult Tobacco Survey questionnaire. Non-probability purposive sampling method was adopted to select the villages. All the households of the villages were visited, and an adult member was selected randomly from each household irrespective of sex. After missing value imputation, 1000 data sets were analysed using statistical software SPSS 19.0 version. Analysis showed that 28.8% of the respondents were current smokers, and 7.8% were past smokers. Among the smokers, 56.3% were habituated with menthol brand cigarette. Logistic regression analysis revealed that age at initiation of smoking before 15 years of age (OR=11. 68, 95% CI: 4.25, 32.10), smoking within five minutes of wake up from sleep (OR=3. 20, 95% CI: 1.35, 7.54), nature of job as business (OR=4. 81, 95% CI: 2.13, 10.86) and service holders (OR= 3.85, 95% CI: 2.07, 7.16) and family size 5 and above (OR=2. 22, 95% CI: 1.25, 3.94) appeared to be important determinants of smoking any menthol brand cigarette (p< 0.05). Menthol is a prominent design feature to attract and retain younger smokers. It does not necessarily make the transition from experimenting with cigarettes, but to encourage early smokers to become a confirmed smoker. So, anti-tobacco public health programme should focus on age-specific community approach.
    Matched MeSH terms: Nicotine
  15. Lim, K.H., Sumarni, M.G., Kee, C.C., Norhamimah, A., Wan Rozita, W.M., Amal, N.M.
    MyJurnal
    Many studies on adolescent smoking have been conducted in Malaysia, but very limited information is available on smoking amongst lower secondary school male students (Forms 1 and 2). We present data from a baseline study in Kota Tinggi District, Johor on the psychosocial factors, stages of smoking acquisition and susceptibility to smoking initiation and their relationship to adolescent smoking. The study is the first wave of a 3-year longitudinal study which was conducted from March 2007 to May 2009, aimed to describe the prevalence of smoking among students in the lower secondary classes. A three stage stratified sampling was performed to obtain a sample. The Bogus Pipeline Method was employed to confirm smoking status. Prevalence of smoking was 35.5%. Smoking prevalence among students of schools located in the Federal Land Development Authority (FELDA) settlement areas (42.9%) was two-fold higher than in the rural and town schools combined (20.29%). Using the Fagerstrom scale, 90% of current smokers had lower addiction to nicotine. Smoking was associated with peer smoking [OR, 4.19 (95% CI, 2.57-6.82)], having a brother smoking [2.17 (1.31-3.61)], parental smoking [1.73 (1.17-2.80)] and locality where respondents attend school [1.94(1.11-3.39)]. The study indicates that, the prevalence of smoking was high in all areas especially FELDA settlement areas. Measures such as teaching of skills to resist social pressure to smoke, establishment of peer support groups and involvement of parents in anti-smoking programs are recommended to curb the high prevalence of smoking among lower secondary school students in Kota Tinggi.
    Matched MeSH terms: Nicotine
  16. Rusdi Abdul Rashid, Muhammad Muhsin Ahmad Zahari, Mohammad Hussain Habil, Noor Zurani Md Haris Robson
    ASEAN Journal of Psychiatry, 2009;10(2):202-209.
    MyJurnal
    Objective: The smoking rate among patients with mental health problem is higher than in the general population. Effective pharmacotherapy to treat nicotine addiction is thus needed to reduce the morbidity and mortality associated with cigarette smoking among these patients. This article reviews the literature on the suitability of varenicline for smokers with mental health problems.
    Methods: A search of the literature was conducted using PubMed from year 2001 to July 2009 using key words varenicline alone and varenicline and mental health. Articles chosen were narrowed to those published in English. The type of articles chosen included clinical trials, metaanalyses, case reports, and review articles.
    Results: The search produced a total of 322 articles on varenicline and 14 articles on varenicline and mental health. Varenicline, a new drug for smoking cessation is an α4β2 partial agonist and partial antagonist at nicotinic acetylcholine receptor. As a partial agonist, varenicline relieves craving and withdrawal symptoms that occur during smoking abstinence and also reduce the rewarding effects of smoking in patients who relapse. However, at present, there is concern regarding the neuropsychiatric side effects such as aggressive behaviour, suicidal ideation, mania and depression associated with varenicline use in patients with mental health problems, but these reports did not show a causal-link or lack of link between these symptoms and varenicline.
    Conclusion: Current available data support the effectiveness of varenicline to treat nicotine dependence. However its safety among smokers with mental health problems remains to be elucidated. At present, further safety assessment is needed in this patient population. Until new data is available regarding the safety of varenicline in these populations, psychiatrists and physicians prescribing this medication should be extra cautious and monitor for possible psychiatric side effects when prescribing this medication to patients with pre-existing psychiatric disorders or have vulnerability to psychoses.
    Matched MeSH terms: Nicotine
  17. Blebil AQ, S Sulaiman SA, A Hassali M, Dujaili JA, Zin AM
    Value Health Reg Issues, 2014 May;3:19-23.
    PMID: 29702926 DOI: 10.1016/j.vhri.2013.09.001
    OBJECTIVES: Assessment of nicotine withdrawal symptoms is an essential part of tobacco dependence treatment. This study aimed to evaluate the psychometric properties of a Malay translated version of the Minnesota Nicotine Withdrawal Scale (MNWS).

    METHODS: The original scale was translated into Malay following the standard guidelines proposed for translation studies. The reliability and validity of the Malay version scale were evaluated on the basis of data collected from 133 participants. The Cronbach's alpha coefficient was calculated to assess the reliability. To validate the psychometric properties of the scale, factor analysis and construct validity were used. This study was conducted at the Quit Smoking Clinic at Penang General Hospital, Penang, Malaysia.

    RESULTS: The translated scale has excellent reliability, with total Cronbach's alpha of 0.91. The test-retest reliability for the scale presented an excellent reliability and stability of the translated scale with Spearman's rank correlation coefficient (r = 0.876; P < 0.001). There was a significant positive correlation between the exhaled carbon monoxide level, Fagerstrom Test for Nicotine Dependence total score, and number of cigarettes smoked per day and the MNWS total score (r = 0.72, 0.68, and 0.68, respectively; P < 0.001). A principal-components analysis with orthogonal rotation yielded a unidimensional model that includes all the items of the MNWS.

    CONCLUSIONS: The Malay version of the MNWS is a reliable and valid measure of withdrawal symptoms as well as the smoking urge, and it is applicable to clinical practice and research study.

    Study site: Quit Smoking Clinic at Penang General Hospital, Penang, Malaysia.
    Matched MeSH terms: Nicotine
  18. Yuhaniza Shafinie Kamsani, Mohd Hamim Rajikin
    MyJurnal
    This review summarizes the impact of tocotrienols (TCTs) as antioxidants in minimizing oxidative stress (OS), particularly in embryos exposed to OS causing agents. OS level is increased, for example, by nicotine, a major alkaloid content in cigarette, which is also a source of exogenous reactive oxygen species (ROS). Increased nicotine-induced OS increases cell stress response, which is a common trigger leading to embryonic cell death. Having more profound anti-oxidative stress effects than its counterpart tocopherol, TCTs improve blastocyst implantation, foetal growth, pregnancy outcome and survival of the neonates affected by nicotine. In reversing cell developmental arrest caused by nicotine-induced OS, TCTs enhances PDK-1 expression in the P13K/Akt pathway and permit embryonic development beyond the 4-cell stage with the production of more morulae. At the cytoskeletal level, TCTs increase the number of nicotine-induced apoptotic cells, through caspase 8 activation in the mitochondria. TCTs facilitate rough endoplasmic reticulum (rER) stress-mediated apoptosis and autophagy, resulting from nicotine-induced OS. Reduced vesicular population in TCT supplemented oocytes on the other hand may suggest reduced secretion of apoptotic cell bodies thus probably minimizing vesicular apoptosis during oocyte maturation. Further extensive research is required to develop TCTs as a tool in specific therapeutic approaches to overcome the detrimental effects of OS.
    Matched MeSH terms: Nicotine
  19. Siti Hajar MH, Zulkefli S, Juwita S, Norhayati MN, Siti Suhaila MY, Rasool AHG, et al.
    PeerJ, 2018;6:e5758.
    PMID: 30356972 DOI: 10.7717/peerj.5758
    Background: Secondhand smoke (SHS) exposure has adverse effects on the cardiovascular system. This study aimed to determine the effects of SHS on the cardiovascular disease biomarkers, namely the metabolic, inflammatory, and oxidative stress markers in healthy adult women.

    Methods: This comparative cross-sectional study was conducted among healthy women. The cases included those women exposed to SHS, and the controls included those women not exposed to SHS. SHS exposure was defined as being exposed to SHS for at least 15 min for 2 days per week. Venous blood was taken to measure the metabolic markers (high molecular weight adiponectin, insulin level, insulin resistance, and nonesterified fatty acids), oxidative stress markers (oxidized low density lipoprotein cholesterol and 8-isoprostane), and inflammatory markers (high-sensitivity C-reactive protein and interleukin-6). A hair nicotine analysis was also performed. An analysis of covariance and a simple linear regression analysis were conducted.

    Results: There were 101 women in the SHS exposure group and 91 women in the non-SHS exposure group. The mean (with standard deviation) of the hair nicotine levels was significantly higher in the SHS exposure group when compared to the non-SHS exposure group [0.22 (0.62) vs. 0.04 (0.11) ng/mg; P = 0.009]. No significant differences were observed in the high molecular weight adiponectin, insulin and insulin resistance, nonesterified fatty acids, 8-isoprostane, oxidized low density lipoprotein cholesterol, interleukin-6, and high-sensitivity C-reactive protein between the two groups. The serum high molecular weight adiponectin was negatively associated with the insulin level and insulin resistance in the women exposed to SHS. However, no significant relationships were seen between the high molecular weight adiponectin and nonesterified fatty acids, 8-isoprostane, oxidized low density lipoprotein cholesterol, high-sensitivity C-reactive protein in the SHS group.

    Discussion: There were no significant differences in the metabolic, oxidative stress, and inflammatory markers between the SHS exposure and non-SHS exposure healthy women. A low serum level of high molecular weight adiponectin was associated with an increased insulin level and resistance in the women exposed to SHS.

    Matched MeSH terms: Nicotine
  20. Yusof NA, Zin FM, Idris NS, Mohammad R
    Korean J Fam Med, 2019 Jul;40(4):254-260.
    PMID: 31109161 DOI: 10.4082/kjfm.18.0016
    BACKGROUND: The rising prevalence of alternative tobacco and nicotine products (ATNPs) use among adolescents is a global concern that has been attributed to the reemergence of preexisting alternative tobacco products and emergence of new ones in the market. This study examined ATNP use among late adolescents. The association between ATNP use and reasons for using them was explored.

    METHODS: This cross-sectional study conducted in 2016 involving 388 late adolescents from six government colleges in Kelantan, Malaysia, aged 18 to 19 years. They were requested to answer self-directed questionnaires with items on sociodemographic information and types of ATNP used. Other variables obtained include the environmental influence and reasons for using the products. Regression analyses between the dependent and independent variables were conducted using IBM SPSS ver. 20.0 (IBM Corp., Armonk, NY, USA).

    RESULTS: The prevalence of ATNP use among late adolescents was 14.4%. The male sex, cigarette smoking status, and peer use were significantly associated with ATNP use. Several reasons for use were not significantly associated with ATNP use: perception of ATNP being less harmful and less addictive compared with cigarettes, curiosity, less expensive than cigarettes, to aid smoking cessation, and pleasurable flavors and taste.

    CONCLUSION: The prevalence of ATNP use among late adolescents studying in government colleges in Kelantan is significant. There is higher perception on ATNP being less harmful and addictive than the conventional cigarette among the users compared with non-users. Significant associations are seen for the male sex, peer use, and concurrent cigarette smoking.

    Matched MeSH terms: Nicotine
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