BACKGROUND & AIMS: OBJECTIVES:Exposure of adults to secondhand smoke (SHS) has immediate adverse effects on the cardiovascular system and causes coronary heart disease. The current study evaluated brief self-report screening measures for accurately identifying adult cardiology patients with clinically significant levels of SHS exposure in need of intervention. DESIGN AND SETTING:A cross-sectional study conducted in a university-affiliated cardiology clinic and cardiology inpatient service. PATIENTS:Participants were 118 non-smoking patients (59% male, mean age=63.6 years, SD=16.8) seeking cardiology services. MAIN OUTCOME MEASURES:Serum cotinine levels and self-reported SHS exposure in the past 24 h and 7 days on 13 adult secondhand exposure to smoke (ASHES) items. RESULTS:A single item assessment of SHS exposure in one's own home in the past 7 days was significantly correlated with serum cotinine levels (r=0.41, p<0.001) with sensitivity ≥75%, specificity >85% and correct classification rates >85% at cotinine cut-off points of >0.215 and >0.80 ng/mL. The item outperformed multi-item scales, an assessment of home smoking rules, and SHS exposure assessed in other residential areas, automobiles and public settings. The sample was less accurate at self-reporting lower levels of SHS exposure (cotinine 0.05-0.215 ng/mL). CONCLUSIONS:The single item ASHES-7d Home screener is brief, assesses recent SHS exposure over a week's time, and yielded the optimal balance of sensitivity and specificity. The current findings support use of the ASHES-7d Home screener to detect SHS exposure and can be easily incorporated into assessment of other major vital signs in cardiology.

背景与目标： 目的：成年人接触二手烟（SHS）对心血管系统有直接的不利影响，并引起冠心病。当前的研究评估了简短的自我报告筛查措施，以准确地识别具有临床意义的SHS暴露水平需要干预的成人心脏病患者。
设计与地点：在大学附属的心脏病诊所和心脏病住院患者服务中进行的横断面研究。
参加者：118位非吸烟患者（男性，占59％，平均年龄= 63.6岁，SD = 16.8）正在寻求心脏病学服务。
主要观察指标：过去24小时和7天，在13项成人二手烟（ASHES）物品中，血清可替宁水平和自我报告的SHS暴露。
结果：过去7天中对自己家中SHS暴露的一项单项评估与血清可替宁水平（r = 0.41，p <0.001）显着相关，敏感性≥75％，特异性> 85％，正确分类率> 85 ％在可替宁截止点> 0.215和> 0.80 / ng / mL时。该项目的表现优于多项目量表，对家庭吸烟规则的评估以及在其他居民区，汽车和公共场所进行的SHS暴露评估。自我报告较低水平的SHS暴露（可卡因0.05-0.215ng / mL）时，样品的准确性较低。
结论：单项ASHES-7d家庭筛查仪是简短的，可评估一周内最近的SHS暴露，并在敏感性和特异性之间取得最佳平衡。目前的发现支持使用ASHES-7d家庭筛查仪检测SHS暴露，并且可以轻松地纳入心脏病学中其他主要生命体征的评估中。

BACKGROUND & AIMS: :The present study investigated whether erythromycin (ERY) reduces cigarette smoke (CS)-induced emphysema in rats and aimed to determine the anti-inflammatory effect of ERY, which may identify potential treatments for chronic obstructive pulmonary disease. Furthermore, the current study focused on the potential effects on the imbalance between matrix metalloprotease (MMP) and anti-MMP activity, the phosphorylation of mitogen-activated protein kinases (MAPKs) and the nuclear factor‑κB (NF‑κB) signaling pathway. Wistar rats were divided into the following three groups (n=12 each): control (ERY vehicle only, without any CS exposure), CS (animals were exposed to CS for 12 weeks) and CS + ERY (animals were exposed to CS for 12 weeks and received 100 mg/kg/day ERY). The recruitment of inflammatory cells into the bronchoalveolar lavage fluid (BALF) and the histopathology of lung tissue from all groups was evaluated to grade the severity of the emphysema. The expression of MMP‑2, MMP‑9 and tissue inhibitor of metalloproteinase‑1 was evaluated by immunohistochemistry and western blotting. The activation of MAPKs, NF‑κB and inhibitor of NF‑κB (IκBα), in lung tissues was examined by western blotting. Treatment with ERY resulted in fewer inflammatory cells and cytokines in the BALF, and fewer emphysema‑associated changes in the lungs compared with control. The stimulus of CS promoted the phosphorylation of extracellular signal‑regulated kinase (ERK)1/2 and p38, but not c‑Jun NH2‑terminal kinase, thereby inducing the activation of the ERK/MAPK signaling pathway in rats. Furthermore, CS exposure increased the expression of NF-κB and decreased the expression of IκBα. The levels of phosphorylated ERK1/2 and p38 were significantly reduced in rats with CS‑induced emphysema when treated with ERY compared with the CS group. The results of the present study therefore indicate that oral administration of ERY may suppress CS‑induced emphysema by regulating inflammatory cytokines and the MMP/anti-MMP imbalance via the MAPK/NF-κB pathway.

背景与目标： ：本研究调查了红霉素（ERY）是否能减少香烟烟​​雾（CS）诱导的大鼠肺气肿，并旨在确定ERY的抗炎作用，从而可能确定慢性阻塞性肺疾病的潜在治疗方法。此外，当前的研究集中在对基质金属蛋白酶（MMP）和抗MMP活性，促分裂原活化蛋白激酶（MAPKs）磷酸化和核因子-κB（NF-κB）信号通路之间不平衡的潜在影响。 Wistar大鼠分为以下三组（每组n = 12）：对照组（仅ERY媒介物，没有任何CS暴露），CS（动物暴露于CS持续12周）和CS ERY（动物暴露于CS持续12周）周，并接受100 mg / kg /天的ERY）。评价炎症细胞进入支气管肺泡灌洗液（BALF）的募集和所有组肺组织的组织病理学，以对肺气肿的严重程度进行分级。通过免疫组织化学和蛋白质印迹法评估了MMP-2，MMP-9和金属蛋白酶-1组织抑制剂的表达。 Western blot检测肺组织中MAPKs，NF-κB和NF-κB抑制剂（IκBα）的活化。与对照相比，用ERY治疗可减少BALF中的炎症细胞和细胞因子，并减少与肺气肿相关的变化。 CS的刺激促进了细胞外信号调节激酶（ERK）1/2和p38的磷酸化，但不促进c-Jun NH2末端激酶的磷酸化，从而诱导了大鼠ERK / MAPK信号通路的激活。此外，CS暴露增加了NF-κB的表达而降低了IκBα的表达。与CS组相比，用ERY治疗时，CS诱发的肺气肿大鼠的磷酸化ERK1 / 2和p38含量显着降低。因此，本研究的结果表明，口服ERY可以通过调节炎症细胞因子和通过MAPK /NF-κB途径引起的MMP /抗MMP失衡来抑制CS诱发的气肿。

BACKGROUND & AIMS: :Common laboratory rats and mice fail to develop persistent, progressive pulmonary inflammation found in chronic obstructive pulmonary disease as a result of tobacco smoke exposure. We hypothesized that spontaneously hypertensive rats would be more susceptible than normal Wistar Kyoto rats to acute tobacco smoke-induced pulmonary inflammation due to impaired apoptosis. Spontaneously hypertensive rats display systemic oxidative stress, inflammation, hypercoagulation, and immunosupression, similar to humans with chronic obstructive pulmonary disease. Male spontaneously hypertensive rats and Wistar Kyoto rats were exposed whole-body to tobacco smoke (total particulate concentration 75-85 mg/m(3)) or filtered air for 6 h/day for 2 or 15 days (3 days/wk). Tobacco smoke caused an increase in bronchoalveolar lavage fluid neutrophils at both time points in each strain. Significantly more neutrophils were noted in spontaneously hypertensive rats at 15 days compared to Wistar Kyoto rats. There was a trend of increase for macrophages in spontaneously hypertensive rats at both time points (significant at 2 days). TUNEL assay detected apoptotic cells in bronchoalveolar lavage fluid and lung tissue sections. The number of apoptotic neutrophils in airway walls and bronchoalveolar lavage fluid increased at 2 days in both strains, but at 15 days the effect was much lower in spontaneously hypertensive rats than in Wistar Kyoto rats. Tobacco smoke induces a greater inflammatory response associated with lower apoptotic neutrophils in the lungs of spontaneously hypertensive rats compared to Wistar Kyoto rats. The spontaneously hypertensive rat may be a more relevant animal model of acute tobacco smoke-induced airway inflammation than other laboratory rats.

背景与目标： ：普通实验室的大鼠和小鼠由于暴露于烟草烟雾而无法发展出在慢性阻塞性肺疾病中发现的持续性进行性肺部炎症。我们假设，由于凋亡受损，自发性高血压大鼠比正常的Wistar Kyoto大鼠更容易受到急性烟草烟雾诱发的肺部炎症的影响。自发性高血压大鼠表现出全身性氧化应激，炎症，高凝和免疫抑制，类似于患有慢性阻塞性肺疾病的人。将雄性自发性高血压大鼠和Wistar Kyoto大鼠全身暴露于烟草烟雾（总颗粒浓度为75-85 mg / m（3））或过滤空气中，每天暴露6小时，持续2或15天（每周3天）。烟草烟雾在每个菌株的两个时间点引起支气管肺泡灌洗液中性粒细胞的增加。与Wistar Kyoto大鼠相比，在第15天的自发性高血压大鼠中发现明显更多的中性粒细胞。自发性高血压大鼠在两个时间点都有巨噬细胞增加的趋势（在2天时显着）。 TUNEL分析检测到了支气管肺泡灌洗液和肺组织切片中的凋亡细胞。两种菌株中，气道壁和支气管肺泡灌洗液中凋亡性中性粒细胞的数量均在第2天增加，但在第15天，自发性高血压大鼠的这种作用远低于Wistar Kyoto大鼠。与Wistar Kyoto大鼠相比，烟草烟雾在自发性高血压大鼠的肺中诱导了更大的炎症反应，并伴有较低的凋亡中性粒细胞。自发性高血压大鼠可能是比其他实验室大鼠更相关的急性烟草烟雾诱发气道炎症的动物模型。

BACKGROUND & AIMS: BACKGROUND:In countries like Turkey where smoking is highly prevalent, children's exposure to tobacco smoke is an important public health problem. The goals of this study were to determine the self-reported environmental tobacco smoke exposure status of primary school students in grades 3 to 5, to verify self-reported exposure levels with data provided from a biomarker of exposure, and to develop methods for preventing school children from passive smoking. METHODS:The study was conducted on 347 primary school students by using a standard questionnaire and urinary cotinine tests. Children with verified ETS exposure were randomly assigned to 2 intervention groups. Two phone interviews were conducted with the parents of the first group regarding their children's passive smoking status and its possible consequences. On the other hand, a brief note concerning urinary cotinine test result was sent to parents of the second group. Nine months after the initial urinary cotinine tests, measurements were repeated in both groups. RESULTS:According to questionnaire data, 59.9% of the study group (208 of 347) were exposed to ETS. Urinary cotinine measurements of children were highly consistent with the self-reported exposure levels (P < 0.001). Two different intervention methods were applied to parents of the exposed children. Control tests suggested a remarkable reduction in the proportion of those children demonstrating a recent exposure to ETS in both groups. Proportions of children with urinary cotinine concentrations 10 ng/ml or lower were 79.5% in Group I and 74.2% in Group II (P > 0.05). CONCLUSION:Self-reported ETS exposure was found to be pretty accurate in the 9-11 age group when checked with urinary cotinine tests. Only informing parents that their children' ETS exposure were confirmed by a laboratory test seems to be very promising in preventing children from ETS.

背景与目标： 背景：在像土耳其这样高度吸烟的国家中，儿童接触烟草烟雾是一个重要的公共卫生问题。这项研究的目的是确定3至5年级的小学生自我报告的环境烟草烟雾暴露状况，以暴露生物标志物提供的数据验证自我报告的暴露水平，并制定预防上学的方法避免被动吸烟的孩子。
方法：采用标准问卷和尿液可替宁测试方法对347名小学生进行了研究。经ETS暴露验证的儿童被随机分为2个干预组。第一组的父母接受了两次电话采访，讨论了他们的孩子的被动吸烟状况及其可能的后果。另一方面，关于尿中可替宁检测结果的简短说明被发送给第二组的父母。最初的尿液可替宁测试后9个月，两组均进行了重复测量。
结果：根据问卷调查数据，研究组中有59.9％（347人中的208人）暴露于ETS中。儿童尿液中可替宁的含量与自我报告的暴露水平高度一致（P <0.001）。对接触儿童的父母采用了两种不同的干预方法。对照测试表明，这两组儿童中最近暴露于ETS的儿童比例显着降低。尿可替宁浓度在10 ng / ml或以下的儿童比例在第一组中为79.5％，在第二组中为74.2％（P> 0.05）。
结论：通过尿液可替宁测试检查，在9-11岁年龄段的人群中，自我报告的ETS暴露是相当准确的。仅告知父母他们的孩子的ETS暴露已通过实验室测试证实，对于预防儿童的ETS似乎很有希望。

BACKGROUND & AIMS: :To investigate whether the effects of in utero exposure to maternal smoking and environmental tobacco smoke (ETS) exposure on lung function vary by sex or asthma status, we examined medical history and tobacco smoke exposure data for 5,263 participants in the Children's Health Study. At study enrollment, parents or guardians of each subject completed a questionnaire, and lung function was measured spirometrically with maximum forced expiratory flow-volume maneuvers. To assess the in utero effects of maternal smoking and ETS exposure on lung function, we used regression splines that accounted for the nonlinear relationship between pulmonary function, height, and age. In utero exposure to maternal smoking was independently associated with deficits in lung function that were larger for children with asthma. Boys and girls with a history of in utero exposure to maternal smoking showed deficits in maximum midexpiratory flow (MMEF) and a decrease in the FEV(1)/FVC ratio. As compared with children without asthma, boys with asthma had significantly larger deficits from in utero exposure in FVC, MMEF, and FEV(1)/FVC, and girls with asthma had larger decreases in FEV(1)/FVC. The effect of ETS exposure varied by children's gender and asthma status. Deficits in flows associated with current ETS exposure were present in children with and without asthma but were significant only among children without asthma. Past ETS exposure was associated with reduced FEV(1), MMEF, and FEV(1)/FVC among boys with asthma. In contrast, past ETS exposure was associated with decreased flow rates in girls without asthma. In summary, both in utero exposure to maternal smoking and ETS exposure were associated with persistent deficits in lung function. The effects of in utero exposure were greatest among children with asthma.

背景与目标： ：为了调查子宫内孕产妇吸烟和环境烟草烟雾（ETS）暴露对肺功能的影响是否因性别或哮喘状况而异，我们检查了儿童健康研究中5,263名参与者的病史和烟草烟雾暴露数据。在研究入组时，每个受试者的父母或监护人填写了一份调查表，并以最大的强制呼气流量对肺功能进行了肺活量测定。为了评估孕妇吸烟和ETS暴露对子宫功能的子宫内影响，我们使用了回归样条，该样条解释了肺功能，身高和年龄之间的非线性关系。子宫内母体吸烟与哮喘患儿的肺功能缺陷独立相关。有子宫内孕产妇吸烟史的男孩和女孩显示最大呼气中期流量不足（MMEF）和FEV（1）/ FVC比值降低。与没有哮喘的儿童相比，患有哮喘的男孩在子宫内暴露的FVC，MMEF和FEV（1）/ FVC的赤字明显更大，而患有哮喘的女孩FEV（1）/ FVC的跌幅更大。 ETS暴露的影响因儿童的性别和哮喘状况而异。哮喘患儿和非哮喘患儿当前与ETS暴露相关的血流不足，但仅在哮喘患儿中才有显着性。过去的ETS暴露与哮喘男孩中FEV（1），MMEF和FEV（1）/ FVC降低有关。相比之下，过去的ETS暴露与没有哮喘的女孩的血流量降低相关。总之，子宫内孕妇吸烟和ETS暴露均与持续的肺功能缺陷有关。子宫内暴露对哮喘患儿的影响最大。

BACKGROUND & AIMS: :The Electrically Heated Cigarette Smoking System Series K (EHCSS) produces smoke through the controlled electrical heating of tobacco. Evaluation of the EHCSS was accomplished by comparison with commercial and reference cigarettes, using International Organization for Standardization (ISO) and alternative puffing regimens based on nicotine exposures measured in a short-term clinical study. Using the alternative puffing regimen and compared with conventional cigarettes on a per cigarette basis, the EHCSS had 50-60% reductions in tar and nicotine; at least 90% reductions in carbon monoxide, nitrogen oxides, 1,3-butadiene, isoprene, acrylonitrile, polyaromatic hydrocarbons, hydrogen cyanide, aromatic amines, tobacco specific nitrosamines, and phenol; and least a 40% reduction in 2-nitropropane. Other important smoke constituents in EHCSS smoke were reduced as well. The in vitro studies showed similar large reductions in biological activity. Ames mutagenicity of total particulate matter (TPM) from the EHCSS was reduced by 70-90%; cytotoxicity of the TPM was reduced by approximately 82% and 65% for the gas-vapor phase. In vivo testing under ISO smoking conditions in the mouse skin painting assay demonstrated later dermal tumor onset, lower dermal tumor incidence, reduced dermal tumor multiplicity, and a lower proportion of malignant dermal tumors in EHCSS smoke condensate-exposed mice. Thirty-five day and 90-day nose-only inhalation studies in rats showed reductions in pulmonary inflammation and other biological activity, including histopathological endpoints. We conclude that under the conditions of these in vitro and in vivo studies, the EHCSS demonstrated significantly lower biological activity compared to conventional cigarettes, and may suggest the potential for reductions in human smokers.

背景与目标： ：K系列电加热烟熏系统（EHCSS）通过控制烟草的电加热来产生烟雾。通过使用国际标准化组织（ISO）和基于短期临床研究中测得的尼古丁暴露量的替代抽吸方法，通过与商用和参考卷烟进行比较，对EHCSS进行评估。使用替代的抽吸方法，并与传统卷烟相比，每支卷烟EHCSS的焦油和尼古丁含量降低了50-60％； EHCSS降低了焦油和尼古丁含量。一氧化碳，氮氧化物，1,3-丁二烯，异戊二烯，丙烯腈，聚芳烃，氰化氢，芳族胺，烟草特定的亚硝胺和苯酚至少减少90％;以及至少减少40％的2-硝基丙烷。 EHCSS烟雾中的其他重要烟雾成分也减少了。体外研究显示出类似的生物活性大幅降低。 EHCSS产生的总颗粒物（TPM）的Ames致突变性降低了70-90％；对于气相而言，TPM的细胞毒性降低了约82％和65％。在ISO吸烟条件下进行的小鼠皮肤涂漆测定法中的体内测试表明，在暴露于EHCSS烟雾的冷凝水中的小鼠，其皮肤肿瘤发作较晚，皮肤肿瘤发病率较低，皮肤肿瘤多重性降低以及恶性皮肤肿瘤的比例较低。在大鼠中进行的35天和90天仅鼻吸气研究表明，肺部炎症和其他生物学活性（包括组织病理学终点）降低了。我们得出的结论是，在这些体外和体内研究的条件下，与传统香烟相比，EHCSS具有明显更低的生物活性，并且可能暗示了减少人类吸烟者的潜力。

BACKGROUND & AIMS: Among 740 patients with acute burns who were admitted to our burn center from 1972 through, 1975, thirty-six required upper airway access within the first 24 hours after burn for oral and facial burns or smoke inhalation. Nasotracheal intubation was initially used. Twelve survived; 11 were successfully extubated and one required a tracheostomy. If the patient had not sustained major smoke inhalation, extubation was usually possible without tracheostomy when edema subsided between one and six days after the burn. It is concluded that endotracheal intubation is a satisfactory method of gaining airway control in severe oral and facial burns and in smoke inhalation. The mortality associated with orofacial burns or smoke inhalation is related to the degree of lung damage, patients' s age, and the extent of the burn; it is not related to the method of upper airway control.

背景与目标： 在1972年至1975年进入我们烧伤中心的740例急性烧伤患者中，有36例需要在烧伤后的前24小时内进行口腔和面部烧伤或吸入烟气。最初使用鼻气管插管。十二个幸存下来；成功拔管11例，其中1例需要气管切开术。如果患者未持续大量吸入烟气，则在烧伤后1至6天浮肿消退时，通常无需气管造口术即可拔管。结论是气管插管是在严重的口腔和面部烧伤以及吸入烟气中获得气道控制的令人满意的方法。口腔烧伤或吸入烟尘的死亡率与肺部损伤程度，患者的年龄以及烧伤程度有关。与上呼吸道控制方法无关。

BACKGROUND & AIMS: :4-(Methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) is a carcinogenic compound of cigarette smoke that generates electrophilic intermediates capable of damaging DNA. Recently, we have shown that NNK can modulate mediator production by alveolar macrophages (AM) and bronchial and alveolar epithelial cells, suggesting that cigarette smoke can alter lung immune response. Thus, we investigated the effect of NNK and cigarette smoke extract (CSE) on AM capacity to eliminate tumoral cells. Rat AM cell line, NR8383, was treated with NNK (500 microM) or CSE (3%) and stimulated with lipopolysaccharide (10 ng/ml). The release of cytotoxic mediators, tumor necrosis factor (TNF) and reactive oxygen species (ROS), was measured in cell-free supernatants using ELISA and superoxide anion production. TNF- and ROS-dependent cytotoxicity were studied using a (51)Chromium-release assay and WEHI-164 and P-815 cell lines. Treatment of AM with NNK and CSE for 18 h significantly inhibited AM TNF release. CSE exposure resulted in a significant increase of ROS production, whereas NNK did not. TNF-dependent cytotoxic activity of NR8383 and freshly isolated rat AM was significantly inhibited after treatment with NNK and CSE. Interestingly, although ROS production was stimulated by CSE and not affected by NNK, CSE inhibited AM ROS-dependent cytotoxicity. These results suggest that NNK may be one of the cigarette smoke components responsible for the reduction of pulmonary cytotoxicity. Thus, NNK may have a double pro-carcinogenic effect by contributing to DNA adduct formation and inhibiting AM cytotoxicity against tumoral cells.

背景与目标： ：4-（甲基亚硝胺基）-1-（3-吡啶基）-1-丁酮（NNK）是香烟烟雾的致癌化合物，可产生能够破坏DNA的亲电子中间体。最近，我们已经显示NNK可以调节肺泡巨噬细胞（AM）以及支气管和肺泡上皮细胞的介体产生，这表明香烟烟雾可以改变肺部免疫反应。因此，我们研究了NNK和香烟烟雾提取物（CSE）对AM消除肿瘤细胞能力的影响。用NNK（500 microM）或CSE（3％）处理大鼠AM细胞系NR8383，并用脂多糖（10 ng / ml）刺激。使用ELISA和超氧阴离子产生法在无细胞上清液中测量细胞毒性介质，肿瘤坏死因子（TNF）和活性氧（ROS）的释放。使用（51）铬释放试验以及WEHI-164和P-815细胞系研究了TNF-依赖性和ROS依赖性细胞毒性。用NNK和CSE治疗AM 18小时可显着抑制AM TNF释放。 CSE暴露导致ROS产生显着增加，而NNK则没有。用NNK和CSE处理后，NR8383和新鲜分离的大鼠AM的TNF依赖性细胞毒性活性被显着抑制。有趣的是，尽管CSE刺激了ROS的产生，而不受NNK的影响，但CSE抑制了AM ROS依赖性的细胞毒性。这些结果表明，NNK可能是引起肺细胞毒性降低的香烟烟雾成分之一。因此，通过促进DNA加合物的形成并抑制AM对肿瘤细胞的细胞毒性，NNK可能具有双重致癌作用。

BACKGROUND & AIMS: :BACKGROUND: Indonesia has the second highest smoking prevalence among adult males in the world, and smoking prevalence is increasing among youths.OBJECTIVE: To evaluate the smoke-free policy (SFP), a flagship national tobacco control programme, by providing evidence on geographic distribution, socio-economic disparities and policy determinants of SFP adoption by district in Indonesia.METHODS: We employed spatial and quantitative methods to obtain data respectively on geographic distribution of SFP adoption, and on disparities and associations between national and provincial SFP regulations and SFP adoption by the districts.RESULTS: Twenty-one of 34 provinces, and 345 of 514 districts adopted SFP. We found significant geographic disparities: all districts outside of Papua were up to 6.3 times more likely to adopt the policy and to implement it for a period of up to 3 years longer in duration. We also found significant socio-economic disparities: urban districts, those that were wealthiest and those most educated were respectively 3.9, 9.1 and 2.8 times more likely to adopt the policy. Moreover, districts in provinces that had SFP regulation were 3.2 times more likely to adopt. Finally, the adoption rate in the period after the 2012 national regulation was up to 7.8 times higher than that before.CONCLUSION: In addition to geographic and socio-economic disparities, national and provincial regulations and policies were determinants of SFP adoption.

背景与目标： 背景：印度尼西亚是世界上成年男性中吸烟率第二高的国家，年轻人中吸烟率正在上升。目标：通过提供地理上的证据来评估国家无烟政策的旗舰性无烟政策（SFP）方法：我们采用空间和定量方法分别获得了有关SFP采伐地理分布的数据，以及国家和省级SFP法规与SFP采伐之间的差距和关联的数据结果：34个省中的21个省和514个区中的345个区采用了SFP。我们发现了巨大的地理差异：巴布亚以外的所有地区采用该政策的可能性提高了6.3倍，并且实施该政策的时间最多延长了3年。我们还发现了巨大的社会经济差异：城市，最富有的地区和受教育程度最高的地区，采用该政策的可能性分别高3.9倍，9.1倍和2.8倍。此外，具有SFP法规的省份采用该法规的可能性要高3.2倍。最后，2012年国家法规实施后的采用率是之前的7.8倍。结论：除了地理和社会经济差异外，国家和省级法规政策也是SFP采纳的决定因素。

BACKGROUND & AIMS: :The genotoxic effects of 90-day nose-only exposures to smoke from new cigarettes, which heat but do not burn tobacco (New), or from reference cigarettes, which burn tobacco, were evaluated in Sprague-Dawley rats by examining the cytogenetic endpoints of sister-chromatid exchanges (SCE), chromosome aberrations, and micronuclei in bone-marrow cells. The concentrations of wet total particulate matter (WTPM) and carbon monoxide in the smoke from both cigarette types were similar. The mainstream smoke from both New and reference cigarettes was adjusted to WTPM concentrations of approx. 200 and 400 micrograms/l for low and high smoke exposure. Rats were exposed to smoke 1 h per day, 5 days per week for 13 consecutive weeks. Inhalation of smoke by the exposed animals was confirmed by analysis of blood carboxyhemoglobin and plasma nicotine. Examination of bone-marrow cells following the final day of exposure showed that smoke from neither the New nor reference cigarette induced a positive response in the SCE, chromosome aberration, or micronucleus assays in rats.

背景与目标： ：在Sprague-Dawley大鼠中，通过检查细胞遗传学终点，评估了仅90天鼻饲暴露于加热但不燃烧烟草的新香烟（新）或参考香烟燃烧的烟的遗传毒性作用。染色单体交换（SCE），染色体畸变和骨髓细胞中的微核的变化。两种香烟的烟雾中的湿总颗粒物（WTPM）和一氧化碳的浓度相似。将新卷烟和参考卷烟的主流烟气调节至WTPM浓度约为。 200和400微克/升，适用于低烟量和高烟量。将大鼠每天1小时，每周5天，每天连续13周暴露于烟雾中。通过分析血液中的羧基血红蛋白和血浆尼古丁来确认暴露的动物吸入烟气。暴露的最后一天后对骨髓细胞的检查表明，新香烟和参比香烟中的烟雾均未在大鼠的SCE，染色体畸变或微核试验中诱导阳性反应。

BACKGROUND & AIMS: :As smoke-free car policy is a frontier domain for tobacco control, attitudes to smoke-free private car laws are briefly reviewed. Medline and Google Scholar searches for the period up to mid-November 2008, from English language sources, were undertaken. Studies were included that contained data from national and subnational populations (eg, in states and provinces), but not for smaller administrative units, eg, cities or councils. Jurisdiction, sample size and survey questions were assessed. One reviewer conducted the data extraction and both authors conducted assessments. A total of 15 relevant studies (from 1988) were identified, set in North America, the UK and Australasia. The available data indicates that, for the jurisdictions with data, there is majority public support for laws requiring cars that contain children to be smoke free. There appears to be an increase over time in this support. In five surveys in 2005 or since (in California, New Zealand and Australia), the support from smokers was 77% or more. The high levels of public (and smoker) support for smoke-free car laws found in the studies to date suggest that this can be a relatively non-controversial tobacco control intervention. Survey series on attitudes to such laws are needed, and surveys in jurisdictions where the issue has not been investigated to date.

背景与目标： ：由于无烟汽车政策是烟草控制的前沿领域，因此简要回顾了对无烟私家车法律的态度。 Medline和Google Scholar进行了英语来源的搜索，搜索截止到2008年11月中旬。纳入的研究包含来自国家和地方以下人口的数据（例如，州和省），但不适用于较小的行政单位（例如，城市或议会）。评估了司法管辖区，样本量和调查问题。一位审稿人进行了数据提取，两位作者进行了评估。共确定了15项相关研究（自1988年起），分别在北美，英国和大洋洲进行。现有数据表明，对于有数据的司法管辖区，大多数公众支持法律要求载有儿童的汽车禁止吸烟。随着时间的推移，这种支持似乎有所增加。在2005年或此后的五项调查中（在加利福尼亚，新西兰和澳大利亚），吸烟者的支持率为77％或更多。迄今为止，在研究中发现，公众（和吸烟者）对无烟汽车法律的高度支持表明这可能是相对无争议的烟草控制干预措施。需要对此类法律的态度进行一系列调查，并在迄今尚未对该问题进行调查的辖区中进行调查。

BACKGROUND & AIMS: PURPOSE:Smokers have increased denture stomatitis caused primarily by Candida albicans. The primary aim of this study was to demonstrate the impact of a wide range of nicotine and cigarette smoke condensate (CSC) concentrations on biofilm formation and metabolic activity of C. albicans on acrylic denture material. MATERIALS AND METHODS:C. albicans (ATCC strain 10231) was used. Standardized denture acrylic (PMMA) specimens (total of 135 specimens) were incubated with C. albicans and exposed to nicotine and CSC at different concentrations (0, 0.25, 0.5, 1, 2, 4, 8, 16, and 32 mg/ml) and (0, 0.25, 0.5, 1, 2, and 4 mg/ml), respectively. For each experiment, 3 samples per nicotine and CSC concentration and a total of 45 specimens (27 specimens for the nicotine and 18 specimens for the CSC-treated samples) were used and were selected randomly for each group. The control group consisted of 0 mg/ml of nicotine or CSC. The viability of C. albicans was measured using spiral plating on blood agar plates. The effect of nicotine and CSC concentrations on planktonic cells was were measured using a microplate reader. Metabolic activity of 24-hour-old established C. albicans biofilm exposed to nicotine and CSC for 24 hours in microtiter plates was determined using a 2,3-bis (2-methoxy-4-nitro-5-sulfophenyl)-2H-tetrazolium-carboxanilide (XTT) reduction assay. RESULTS:The viability of C. albicans increased concomitant with increasing concentrations of CSC and nicotine, particularly at 0.5 and 2 mg/ml, respectively. Concentrations of CSC and nicotine above this resulted in an inhibitory effect on C. albicans viability. CSC and nicotine at 4 and 16 mg/ml, respectively, increased C. albicans biofilm metabolic activity. CONCLUSION:Nicotine and CSC up to certain concentrations caused increases in biofilm formation, metabolic activity, viability, and planktonic cell absorbance of C. albicans. This in vitro study demonstrates the effectiveness of tobacco on promoting the growth of C. albicans and suggests their potential contributing factor in C. albicans biofilm related infections in smokers.

背景与目标： 目的：吸烟者增加的假牙口腔炎主要由白色念珠菌引起。这项研究的主要目的是证明各种尼古丁和香烟烟雾冷凝物（CSC）的浓度对丙烯酸假牙材料上白念珠菌生物膜形成和代谢活性的影响。
材料与方法：C．使用白色念珠菌（ATCC菌株10231）。将标准义齿丙烯酸（PMMA）标本（共135个标本）与白色念珠菌一起孵育，并以不同浓度（0、0.25、0.5、1、2、4、8、16和32 mg / ml的尼古丁和CSC暴露） ）和（0、0.25、0.5、1、2和4 mg / ml）。对于每个实验，每个尼古丁和CSC浓度使用3个样品，共使用45个样本（尼古丁为27个样本，CSC处理的样本为18个样本），并随机选择每组。对照组由0 mg / ml尼古丁或CSC组成。使用螺旋琼脂平板在血琼脂平板上测量白色念珠菌的生存力。使用酶标仪测量尼古丁和CSC浓度对浮游细胞的影响。使用2,3-双（2-甲氧基-4-硝基-5-硝基苯基）-2H-四唑鎓测定在微量滴定板中暴露于尼古丁和CSC中24小时的24小时建立的白色念珠菌生物膜的代谢活性-甲酰苯胺（XTT）还原测定。
结果：白色念珠菌的生存能力随着CSC和烟碱浓度的增加而增加，尤其是分别在0.5和2 mg / ml时。高于此浓度的CSC和烟碱会导致对白色念珠菌生存能力的抑制作用。 CSC和尼古丁分别以4和16 mg / ml的浓度增加白色念珠菌的生物膜代谢活性。
结论：高达一定浓度的尼古丁和CSC导致白色念珠菌的生物膜形成，代谢活性，活力和浮游细胞吸收增加。这项体外研究证明了烟草在促进白色念珠菌生长方面的有效性，并表明了烟草在吸烟者中白色念珠菌生物膜相关感染的潜在影响因素。

BACKGROUND & AIMS: :Phosphatase activity of the major serine threonine phosphatase, protein phosphatase 2A (PP2A), is blunted in the airways of individuals with chronic obstructive pulmonary disease (COPD), which results in heightened inflammation and proteolytic responses. The objective of this study was to investigate how PP2A activity is modulated in COPD airways. PP2A activity and endogenous inhibitors of PP2A were investigated in animal and cell models of COPD. In primary human bronchial epithelial (HBE) cells isolated from smokers and donors with COPD, we observed enhanced expression of cancerous inhibitor of PP2A (CIP2A), an oncoprotein encoded by the KIAA1524 gene, compared with cells from nonsmokers. CIP2A expression was induced by chronic cigarette smoke exposure in mice that coincided with a reduction in PP2A activity, airspace enlargements, and loss of lung function, as determined by PP2A phosphatase activity, mean linear intercept analysis, and forced expiratory volume in 0.05 second/forced vital capacity. Modulating CIP2A expression in HBE cells by silencing RNA or chemically with erlotinib enhanced PP2A activity, reduced extracellular-signal-regulated kinase phosphorylation, and reduced the responses of matrix metalloproteinases 1 and 9 in HBE cells isolated from subjects with COPD. Enhanced epithelial growth factor receptor responses in cells from subjects with COPD were observed to modulate CIP2A expression levels. Our study indicates that chronic cigarette smoke induction of epithelial growth factor receptor signaling and CIP2A expression can impair PP2A responses that are associated with loss of lung function and enhancement of proteolytic responses. Augmenting PP2A activity by manipulating CIP2A expression may represent a feasible therapeutic approach to counter smoke-induced lung disease.

背景与目标： 慢性阻塞性肺疾病（COPD）个体的气道中主要丝氨酸苏氨酸磷酸酶2A（PP2A）的磷酸酶活性减弱，导致炎症和蛋白水解反应增强。这项研究的目的是调查如何在COPD气道中调节PP2A活性。在COPD的动物和细胞模型中研究了PP2A活性和PP2A的内源性抑制剂。在从患有COPD的吸烟者和供体中分离出的原代人支气管上皮（HBE）细胞中，我们观察到与不吸烟者相比，由KIAA1524基因编码的癌蛋白PP2A（CIP2A）的癌性抑制剂的表达有所提高。 CIP2A表达是由小鼠长期吸烟引起的，与PP2A活性降低，空域扩大和肺功能丧失相吻合（PP2A磷酸酶活性，平均线性截距分析和强制呼气量以0.05秒/强迫测定）肺活量。通过沉默RNA或化学作用与厄洛替尼调节HBE细胞中的CIP2A表达，可增强PP2A活性，减少细胞外信号调节的激酶磷酸化，并减少从患有COPD的受试者中分离的HBE细胞中基质金属蛋白酶1和9的反应。观察到来自患有COPD的受试者的细胞中增强的上皮生长因子受体应答调节了CIP2A表达水平。我们的研究表明，长期吸烟诱导上皮生长因子受体信号传导和CIP2A表达可削弱与肺功能丧失和蛋白水解反应增强相关的PP2A反应。通过控制CIP2A的表达来增强PP2A的活性可能是对抗烟尘诱发的肺部疾病的一种可行的治疗方法。

BACKGROUND & AIMS: :Cigarette smoke (CS) is the leading risk factor to develop COPD. Therefore, the pathologic effects of whole CS on the differentiation of primary small airway epithelial cells (SAEC) were investigated, using cells from three healthy donors and three COPD patients, cultured under ALI (air-liquid interface) conditions. The analysis of the epithelial physiology demonstrated that CS impaired barrier formation and reduced cilia beat activity. Although, COPD-derived ALI cultures preserved some features known from COPD patients, CS-induced effects were similarly pronounced in ALI cultures from patients compared to healthy controls. RNA sequencing analyses revealed the deregulation of marker genes for basal and secretory cells upon CS exposure. The comparison between gene signatures obtained from the in vitro model (CS vs. air) with a published data set from human epithelial brushes (smoker vs. non-smoker) revealed a high degree of similarity between deregulated genes and pathways induced by CS. Taken together, whole cigarette smoke alters the differentiation of small airway basal cells in vitro. The established model showed a good translatability to the situation in vivo. Thus, the model can help to identify and test novel therapeutic approaches to restore the impaired epithelial repair mechanisms in COPD, which is still a high medical need.

背景与目标： ：香烟烟雾（CS）是发展COPD的主要危险因素。因此，使用来自三名健康供体和三名COPD患者的细胞，在ALI（气液界面）条件下培养，研究了整个CS对原代小气道上皮细胞（SAEC）分化的病理学影响。上皮生理学分析表明，CS损害了屏障形成并降低了纤毛搏动活性。尽管源自COPD的ALI培养物保留了COPD患者已知的某些特征，但与健康对照相比，来自患者的ALI培养物中CS诱导的作用相似。 RNA测序分析揭示了CS暴露后基底细胞和分泌细胞标记基因的失控。从体外模型（CS与空气）获得的基因特征与人类上皮刷（吸烟者与非吸烟者）的公开数据集之间的比较表明，失调基因与CS诱导的途径之间存在高度相似性。总体而言，香烟烟雾在体外会改变小气道基底细胞的分化。建立的模型对体内情况显示出良好的可翻译性。因此，该模型可以帮助鉴定和测试新颖的治疗方法以恢复COPD中受损的上皮修复机制，这仍然是高度医疗需求。

BACKGROUND & AIMS: -2

背景与目标： -2