配施饼肥对烤烟叶片含氮化合物代谢及酶活性的影响

通过饼肥用量盆栽试验,研究了K326中部叶在不同生育时期硝酸还原酶和中上部叶片含氮化合物总氮、烟碱、可溶性蛋白质和游离氨基酸含量的变化规律.结果表明,硝酸还原酶随着有机肥施用量的增加酶活性呈增加趋势,中上部叶片的总氮和烟碱含量随有机肥的增加呈上升的趋势,而蛋白质含量则呈下降的趋势,有机肥可以促进游离氨基酸含量的提高.     

烤烟烟碱合成及农艺调节效应研究进展

从烟碱合成的部位、前体物质、信号物质以及烟碱在器官间、叶位间和叶片中的分布阐述了烤烟烟碱合成和分布的规律,并对氮、磷、钾等矿质元素,品种、打顶留叶、密度、地膜覆盖、灌溉、成熟度、外源调节物质、环切和断根等农艺措施以及土壤、气候、海拔等环境因子对烤烟烟碱合成的影响进行了综述.     

打顶时期对烤烟根系活力及烟碱积累规律的影响

对不同打顶时期烤烟根系活力及烟碱积累规律进行了研究。结果表明,根系活力和根系烟碱含量呈显著的正相关关系。根系活力和根系烟碱含量均随打顶时期的推迟增加幅度降低,且增至最高值后下降较快。打顶时期与烤烟中上部叶烟碱含量有显著的负相关关系。中部叶烟碱含量以扣心打顶处理最高,烟碱积累强度高峰均出现在打顶后20d前后。上部叶烟碱积累强度高峰均出现在移栽后80d,且随打顶时期推迟烟碱积累强度高峰依次下降,烟碱含量也依次降低,每推迟一天打顶烟碱含量就下降0.0504%。     

烤烟（40级）烟叶焦油量和烟气烟碱的测定分析

通过对烤烟(40级)各等级烟叶焦油含量和烟气烟碱的测定,取得了一套较为完整的分析数据。分析研究了烟叶部位、颜色、成熟度、等级等因素与焦油量和烟气烟碱的关系,找出了规律性。为合理利用烟叶资源,指导配方设计,提高卷烟质量及开发高质量低焦油安全卷烟新产品提供了科学依据。     

Reducing the addictiveness of cigarettes

OBJECTIVE—To assess the feasibility of reducing tobacco-caused disease by gradually removing nicotine from cigarettes until they would not be effective causes of nicotine addiction.
DATA SOURCES—Issues posed by such an approach, and potential solutions, were identified from analysis of literature published by the US Food and Drug Administration (FDA) in its 1996 Tobacco Rule, comments of the tobacco industry and other institutions and individuals on the rule, review of the reference lists of relevant journal articles, other government publications, and presentations made at scientific conferences.
DATA SYNTHESIS—The role of nicotine in causing and sustaining tobacco use was evaluated to project the impact of a nicotine reduction strategy on initiation and maintenance of, and relapse to, tobacco use. A range of potential concerns and barriers was addressed, including the technical feasibility of reducing cigarette nicotine content to non-addictive levels, the possibility that compensatory smoking would reduce potential health benefits, and whether such an approach would foster illicit ("black market") tobacco sales. Education, treatment, and research needs to enable a nicotine reduction strategy were also addressed. The Council on Scientific Affairs came to the following conclusions: (a) gradually eliminating nicotine from cigarettes is technically feasible; (b) a nicotine reduction strategy holds great promise in preventing adolescent tobacco addiction and assisting the millions of current cigarette smokers in their efforts to quit using tobacco products; (c) potential problems such as compensatory over-smoking of denicotinised cigarettes and black market sales could be minimised by providing alternate forms of nicotine delivery with less or little risk to health, as part of expanded access to treatment; and (d) such a strategy would need to be accompanied by relevant research and increased efforts to educate consumers and health professionals about tobacco and health.
CONCLUSIONS—The council recommends the following: (a) that cessation of tobacco use should be the goal for all tobacco users; (b) that the American Medical Association continue to support FDA authority over tobacco products, and FDA classification of nicotine as a drug and tobacco products as drug-delivery devices; (c) that research be encouraged on cigarette modifications that may result in less addicting cigarettes; (d) that the FDA require that the addictiveness of cigarettes be reduced within 5-10 years; (e) expanded surveillance to monitor trends in the use of tobacco products and other nicotine-containing products; (f) expanded access to smoking cessation treatment, and strengthening of the treatment infrastructure; and (g) more accurate labelling of tobacco products, including a more meaningful and understandable indication of nicotine content.


     

Nicotine replacement therapy, professional therapy, snuff use and tobacco smoking: a study of smoking cessation strategies in southern Sweden

Objectives

The strategies used to support smoking cessation among quitters were investigated according to year of smoking cessation and sociodemographic characteristics.

Methods

The 2004 public health survey in Skåne, Sweden, is a cross‐sectional study. A total of 27 757 people aged 18–80 answered a postal questionnaire. The participation rate was 59%. Different strategies to support smoking cessation—that is, no therapy, nicotine replacement (NRT), professional therapy and snus (snuff) use, were investigated among quitters according to year of smoking cessation, and demographic and socioeconomic characteristics.

Results

14.9% of the men and 18.1% of the women were daily smokers. The prevalence of daily snus use was 19.5% among men but only 2.3% among women. Stratifying the data according to year of smoking cessation (1938–2004) revealed a significant increase in active smoking cessation strategies such as NRT, professional therapy and snus use. NRT was more common among women (23.6%) than men (14.8%) among smokers who quit in 2000–4, but snus use was more common among men (30.4% versus 8.7%). No replacement or other therapy at all was significantly more common among women (63.6%) than men (52.1%). People aged 35–80 years used more nicotine replacement than people aged 18–34, while men aged 18–34 used snus to quit smoking significantly more than men aged 55–80.

Conclusions

Snus is used commonly among men as a support for smoking cessation in Sweden. Women use pharmacological NRT to a greater extent, but this can probably not compensate for the much higher extent of snuff use as a cessation strategy among men.     

Regulation of Cisplatin Resistance in Lung Cancer Cells by Nicotine,BDNF, and a β-Adrenergic Receptor Blocker

It is well-recognized that cigarette smoking is a primary risk factor in the development of non-small cell lung cancer (NSCLC), known to account for ~80% of all lung cancers with nicotine recognized as the major addictive component. In investigating the effect of nicotine, brain-derived neurotrophic factor (BDNF), and the β-adrenergic receptor blocker, propranolol, on sensitivity of NSCLC cell lines, A549 and H1299, to cisplatin, we found increased cell viability, and enhanced cisplatin resistance with nicotine and/or BDNF treatment while opposite effects were found upon treatment with propranolol. Cell treatment with epinephrine or nicotine led to EGFR and IGF-1R activation, effects opposite to those found with propranolol. Blocking EGFR and IGF-1R activation increased cell sensitivity to cisplatin in both cell lines. PI3K and AKT activities were upregulated by nicotine or BDNF and downregulated by cell treatment with inhibitors against EGFR and IGF-1R and by propranolol. Apoptosis and cell sensitivity to cisplatin increased upon co-treatment of cells with cisplatin and inhibitors against PI3K or AKT. Our findings shed light on an interplay between nicotine, BDNF, and β-Adrenergic receptor signaling in regulating survival of lung cancer cells and chemoresistance which can likely expand therapeutic opportunities that target this regulatory network in the future.     

The Impact of Nicotine along with Oral Contraceptive Exposure on Brain Fatty Acid Metabolism in Female Rats

Smoking-derived nicotine (N) and oral contraceptive (OC) synergistically exacerbate ischemic brain damage in females, and the underlying mechanisms remain elusive. In a previous study, we showed that N + OC exposure altered brain glucose metabolism in females. Since lipid metabolism complements glycolysis, the current study aims to examine the metabolic fingerprint of fatty acids in the brain of female rats exposed to N+/−OC. Adolescent and adult Sprague–Dawley female rats were randomly (n = 8 per group) exposed to either saline or N (4.5 mg/kg) +/−OC (combined OC or placebo delivered via oral gavage) for 16–21 days. Following exposure, brain tissue was harvested for unbiased metabolomic analysis (performed by Metabolon Inc., Morrisville, NC, USA) and the metabolomic profile changes were complemented with Western blot analysis of key enzymes in the lipid pathway. Metabolomic data showed significant accumulation of fatty acids and phosphatidylcholine (PC) metabolites in the brain. Adolescent, more so than adult females, exposed to N + OC showed significant increases in carnitine-conjugated fatty acid metabolites compared to saline control animals. These changes in fatty acyl carnitines were accompanied by an increase in a subset of free fatty acids, suggesting elevated fatty acid β-oxidation in the mitochondria to meet energy demand. In support, β-hydroxybutyrate was significantly lower in N + OC exposure groups in adolescent animals, implying a complete shunting of acetyl CoA for energy production via the TCA cycle. The reported changes in fatty acids and PC metabolism due to N + OC could inhibit post-translational palmitoylation of membrane proteins and synaptic vesicle formation, respectively, thus exacerbating ischemic brain damage in female rats.