雄激素对前列腺癌细胞内游离钙离子浓度的影响

目的 探讨5α-双氢睾酮(DHT)对前列腺癌LNCaP细胞内游离钙离子浓度([Ca2+]i)的影响及其机制.方法 应用Fura-2/乙酸甲酯(Fura-2/AM)Ca2+荧光探针法结合MiraCal荧光成像系统实时检测不同浓度的DHT刺激以及Ca2+通道阻滞剂干预后LNCaP细胞[Ca2+]i的变化.结果 DHT能快速诱导[Ca2+]i升高,在20 s～3 min升至峰值.DHT浓度为1、10、100和1000nmol/L时能诱导[Ca2+]i分别从基础值(28±5)、(29±5)、(28±4)和(28±9)nmol/L上升至峰值31±3(P＞0.05)、65±9(P＜0.01)、193±33(P＜0.001)和(208±42)nmol/L(P＜0.001).DHT浓度为100和1000 mol/L时,[Ca2+]i峰值间差异无统计学意义(P＞0.05).细胞外液无Ca2+时,1000 nmol/L DHT未能诱导[Ca2+]i升高.细胞膜L-型电压门控Ca2+通道阻滞剂维拉帕米(50μmol/L)、地尔硫卓(100 μmol/L)或硝苯地平(5 mmol/L)37℃孵育细胞5 min后,能完全抑制1000nmol/L DHT诱导的[Ca2+]i升高.磷脂酶C抑制剂新霉素(1 mmol/L)37 ℃孵育细胞5 min或兰尼定受体阻滞剂普鲁卡因(50 mmol/L)37℃孵育细胞3 min后,对1000 nmol/L DHT诱导的[Ca2+]i升高没有影响.结论 DHT可快速、剂量依赖性诱导LNCaP细胞[Ca2+]i升高;DHT诱导LN-CaP细胞[Ca2+]i的升高是细胞外Ca2+经细胞膜L-型电压门控Ca2+通道流入细胞内实现的,细胞内贮钙库未释放Ca2+.     

烟酰胺腺嘌呤二核苷酸对布比卡因所致神经细胞毒性的影响

目的 明确布比卡因是否导致SH-SY5Y细胞内烟酰胺腺嘌呤二核苷酸(nicotinamide adenine dinucleotide,NAD)水平降低,以及NAD水平降低是否与布比卡因神经细胞毒性有关.方法 以1 mmol/L布比卡因培养液处理SH-SY5Y细胞30 min～7 h,检测细胞内NAD含量及细胞活性;以1～10 mmol/L布比卡因处理细胞30 min,检测细胞内NAD含量及细胞活性;于5 mmol/L布比卡因处理细胞30 min前后,以不同NAD培养液预处理、后处理SH-SY5Y细胞30 min,检测细胞内NAD水平的变化及细胞活性.结果 1 mmol/L布比卡因处理后3h,细胞内NAD水平开始下降,至处理7h,细胞内NAD水平降至处理前的(28±8)％;2、5、10 mmol/L布比卡因处理30 min后,细胞内NAD水平分别降至对照组的(22±3)％、(26±7)％及(16±14)％,明显低于对照组(P＜0.05).1 mmol/L布比卡因处理后各时点细胞存活率差异无统计学意义(P＞0.05);1～10 mmol/L布比卡因处理后,细胞存活率随着布比卡因浓度的增高而降低,2、5、10 mmol/L布比卡因组细胞存活率分别降至对照组的(49±9)％、(36±16)％及(26±-4)％(P＜0.05).以2.50、5.00、10.00 mmol/L NAD预处理的细胞,其细胞内NAD水平分别达到对照组的(86±12)％、(89±12)％及(105±59)％,明显高于单独以布比卡因处理的细胞(P＜0.05).以不同浓度NAD预处理或后处理干预后,细胞存活率明显高于单独以5 mmol/L布比卡因处理的细胞,且预处理效果好于后处理(P＜0.05).结论 布比卡因引起神经细胞毒性与NAD水平下降有关,外源性NAD能提升细胞内NAD水平,且能减轻布比卡因的细胞毒性.     

钙浓度变化对体外培养人表皮角质细胞增殖的影响

目的:比较不同钙浓度培养的人表皮角质细胞(HEKs)增殖能力的差异,确定体外培养表皮角质细胞的最适钙浓度.方法:根据培养液中CaCl2浓度不同,将HEKs分为无钙培养组和0.1、0.3、0.5、1.0 mmol/L CaCl2培养组.细胞培养3 h后,加钙离子荧光染料Fluo-3-AM,显微镜观察细胞内的荧光强度,以反映细胞内钙离子浓度的变化;细胞培养2 d后加Hochest33258核染液,荧光显微镜下观察细胞生长形态;培养3 d时镜下观察细胞的生长情况,并分别用流式细胞术和MTT法分析细胞的增殖情况.结果:钙培养可使细胞内钙离子浓度增加,表现为细胞内Fluo-3-AM荧光强度增强,且随着CaCl2浓度的增加,荧光强度亦随之增加;在钙浓度为0.3mmol/L时,细胞的增殖指数最高,为(51.98±14.31)%,增殖活性最强;0.1mmol/L组次之;随着钙浓度的增加,细胞的增殖指数下降,增殖活性受到抑制,0.5～1.0mmol/L钙培养组的增殖指数和增殖活性均明显低于无钙培养组(P均<0.01).结论:不同钙浓度培养影响表皮角质细胞的增殖能力,钙浓度为0.3 mmol/L时细胞的增殖能力最强.     

纳洛酮复合吗啡对胃癌MGC-803细胞生长的影响

本研究旨在观察纳洛酮复合吗啡对胃癌细胞生长的影响,现报道如下. 一、材料与方法 1.细胞培养及分组:人胃癌MGC-803细胞接种在6孔或96孔培养板中,分为4组,每组54孔.对照组(C组)不加任何药物;吗啡组(M组)或纳洛酮组(N组)分别在培养液中加入吗啡(东北制药集团公司沈阳第一制药厂,批号:080701-1)或纳洛酮(北京华素制药股份有限公司,批号:1107131),使药物的终质量浓度分别为0.10 mmol/L或0.01 mmol/L;吗啡+纳洛酮组(MN组)则先在培养液加入纳洛酮,使其终质量浓度为0.010 mmol/L,孵育30 min后再将吗啡加入培养液中使其浓度为0.1 mmol/L继续孵育.     

5-氨基乙酰丙酸光动力学疗法对两种人卵巢癌细胞的体外杀伤作用

目的：探讨5-氨基乙酰丙酸（5-ALA）光动力学疗法（photodynamic therapy,PDT）对体外培养人卵巢癌SKOV3和AO细胞的杀伤作用。方法：于体外培养的SKOV3和AO细胞分别加入不同浓度的5-ALA（0．1、0．5、1．0、2．5、12．5mmol／L）孵育4h,以波长为630nm的半导体激光进行照射,照射能量密度分别为0．1、0．5、2．5、12．5J／cm^2。用四唑盐（MTT）比色法测定细胞存活率,并与单纯药物对照组（不同浓度5ALA孵育、无光照）、单纯光照组（无5-ALA孵育、不同能量密度光照）与阴性对照组（无药物孵育、无光照）进行比较。计算5ALA—PDT对SKOV3和AO细胞的半数杀伤浓度（IC50）。结果：5-ALA—PDT处理后两种卵巢癌细胞存活率均明显下降（P〈0．05）,提示5ALA—PDT对体外培养的人卵巢癌SKOV3和AO细胞均有杀伤作用,其杀伤作用随5-ALA的浓度和激光能量密度增加而增加,当5-ALA浓度超过2．5mmol／L或照射能量密度超过2．5J／cm^2时细胞存活率变化不明显。单纯药物对照组、单纯光照组的细胞存活率与阴性对照组相比差异无显著性（P〉0．05）。5-ALA-PDT对两种卵巢癌细胞杀伤效应强弱不同,对SKOV3及AO细胞的半抑制浓度（IC50）分别为0．34mmol／L和2．50mmol／L,两者差异有显著性（P〈0．05）。结论：5-ALA-PDT可有效杀伤体外培养的人卵巢癌细胞SKOV3和AO细胞,且对两种细胞的杀伤作用有差异,对SKOV3细胞株的杀伤效应要强于AO细胞株。     

p38丝裂原活化蛋白激酶在罗哌卡因致SH-SY5Y细胞凋亡中的作用

目的 评价p38丝裂原活化蛋白激酶(p38MAPK)在罗哌卡因致SH-SY5Y细胞凋亡中的作用,以探讨罗哌卡因诱发神经毒性的机制.方法 采用随机数字表法,将SH-SY5Y细胞随机分为4组(n=18):正常对照组(C组)、10 μmol/L p38MAPK特异性抑制剂SB203580组(SB组)、3 mmol/L罗哌卡因组(R组)、10 μmol/L SB203580+3 mmol/L罗哌卡因组(SB+R组).C组在细胞培养液中继续培养；SB组在含10 μmol/L SB203580培养液中孵育；R组在含3 mmol/L罗哌卡因的培养液中孵育；SB+R组在含10 μmol/L SB203580的培养液中孵育30 min后,用含3mmol/L罗哌卡因的培养液继续孵育.各组细胞培养或罗哌卡因孵育4 h后采用流式细胞仪检测细胞内活性氧(ROS)水平和细胞凋亡率,采用Western blot法检测p38MAPK和磷酸化p38MAPK(p-p38MAPK)的表达,采用MTT法检测细胞活力.结果 与C组比较,R组和SB+R组ROS水平升高,p-p38MAPK表达上调,细胞活力降低,细胞凋亡率升高(P＜0.01),SB组上述指标差异无统计学意义(P＞0.05)；与R组比较,SB组p-p38MAPK表达下调,细胞活力升高,细胞凋亡率降低(P＜0.01).四组p38MAPK表达水平差异无统计学意义(P＞0.05).结论 罗哌卡因致SH-SY5Y细胞凋亡作用的机制部分与p38MAPK的激活有关.     

Oligofectamine介导转录因子SP1诱骗性寡核苷酸转染猪内皮细胞系条件的优化研究

目的确定SP1诱骗性寡核苷酸(Decoy Oligodeoxynucleotides,ODNs)在Oligofectamine介导下转染猪血管内皮细胞系SV-40-PED的最佳转染条件和效果。方法以SV-40-PED为转染对象,在6孔培养板中,接种SV-40-PED细胞2×105/孔,将4μlOligofectamine和不同浓度的SP1ODNs(2.5、5.0、7.5、10.0和12.5μl)分别溶于100μl无血清、无抗生素的DMEM培养基,室温放置20min后转染细胞,SP1ODNs最终浓度分别为50、100、150、200和250nmol/L、转染26h检测不同浓度转染情况,确定最佳SP1ODNs与Oligofectamine的比率、转染时间;流式细胞仪检测细胞内的相对荧光强度及摄取率评价转染效率;荧光显微镜观察细胞内荧光分布;测定细胞上清乳酸脱氢酶(lactate dehydrogenase,LDH)含量,观察细胞损伤情况。结果SV-40-PED在Oligofectamine的介导下可以摄取SP1ODNs。SP1ODNs终浓度为50、100、150nmol/L组细胞形态无明显变化,终浓度为200、250nmol/L组细胞收缩、变圆后逐渐恢复;SP1ODNs终浓度为250nmol/L时,转染26h时细胞形态也无明显变化,48、72h时有细胞漂浮现象。荧光下观察,转染成功各组荧光物质分布于细胞核内,其中SP1ODNs终浓度为200、250nmol/L组可见清晰核仁,浓度越高,荧光强度越强,细胞内荧光物质主要聚集于细胞核。SP1ODNs终浓度为250nmol/L时,转染72h组LDH浓度为137.12±3.92U/L,显著高于26h的49.61±17.13U/L和48h的120.26±8.42U/L,均有统计学意义(P<0.01);当转染时间为26h时,各浓度组上清液LDH值差异无统计学意义(P>0.05)。结论SP1ODNs终浓度为250nmol/L、转染26h时可以为SV-40-PED转染提供良好效果。     

乙酰左旋肉碱预处理对低氧低糖诱导PC12细胞凋亡的影响

目的 评价乙酰左旋肉碱预处理对低氧低糖诱导PC12细胞凋亡的影响.方法 PC12细胞接种于96孔板中,采用随机数字表法,将细胞随机分为5组(n=6):对照组(C组)、细胞损伤组(Ⅰ组)和不同浓度乙酰左旋肉碱预处理组(A1-3组).C组加入含葡萄糖4.5 g/L的DMEM溶液孵育3h;Ⅰ组加入含葡萄糖0.5 g/L和Na2SO4 3 mmol/L的DMEM溶液孵育3h;A1-3组分别加入0.2、0.4和0.6 mmol/L乙酰左旋肉碱孵育24h,然后加入含葡萄糖0.5 g/L和Na2S2O4 3mmol/L的DMEM溶液孵育3h.采用MTT法检测细胞活力,采用TUNEL法检测细胞凋亡率,测定细胞SOD和ATP酶的活性和MDA含量.结果 与C组比较,Ⅰ组细胞活力降低,细胞凋亡率升高,SOD和ATP酶的活性降低,MDA含量增加(P＜0.05),A1-3组细胞活力、细胞凋亡率、SOD和ATP酶的活性和MDA含量差异无统计学意义(P＞0.05);与Ⅰ组比较,A1-3组细胞活力升高,细胞凋亡率降低,SOD和ATP酶的活性升高,MDA含量下降(P＜ 0.05);A1-3组间细胞活力、细胞凋亡率、SOD和ATP酶的活性和MDA含量比较差异无统计学意义(P＞0.05).结论 乙酰左旋肉碱预处理可通过抑制细胞凋亡,减轻低氧低糖诱导PC12细胞损伤.     

T-型钙通道在利多卡因致神经母细胞瘤SH-SY5Y细胞损伤中的作用

目的 探讨T-型钙通道在利多卡因致神经母细胞瘤SH-SY5Y细胞损伤中的作用.方法 SH-SY5Y细胞离体培养后,采用随机数字表法,将SH-SY5Y细胞随机分为4组,每组66孔,正常对照组(C组):SH-SY5Y细胞继续培养24 h;米贝地尔+SH-SY5Y细胞组(M组):培养液中加入T-型钙通道阻断剂米贝地尔,终浓度5 μmol/L,孵育24 h;利多卡因+SH-SY5Y细胞组(L组):培养液中加入利多卡因,终浓度10 mmol/L,孵育24 h;米贝地尔+利多卡因+SH-SYSY细胞组(ML组):培养液中加入米贝地尔和利多卡因,终浓度分别为5 μmol/L、10 mmol/L,孵育24 h.于开始培养或孵育时(T0)、培养或孵育1、6、12和24 h时测定SH-SY5Y细胞活力和凋亡率,孵育24 h时观察SH-SY5Y细胞形态学.结果 与C组比较,L组和ML组SH-SY5Y细胞活力降低,凋亡率升高(P＜0.05),M组差异无统计学意义(P＞0.05);与M组比较,L组和ML组SH-SY5Y细胞活力降低,凋亡率升高(P＜0.05);与L组比较,ML组SH-SYSY细胞活力升高,凋亡率降低(P＜0.05).L组SH-SY5Y细胞形态学发生改变,ML组SH-SY5Y细胞形态学改变较L组减轻.结论 T-型钙通道参与了利多卡因导致的神经细胞损伤.

Abstract：

Objective To investigate the role of T-type calcium channel in lidocaine-induced neuronal cytotoxicity . Methods SH-SYSY cell line was a gift from cell biology laboratory of our medical university. The cells were cultured in DMEM liquid culture medium at 37℃ in incubator filled with 5% CO2 , and randomly divided into 4 groups ( n = 66 each) : control group (group C)and M, L and ML groups were exposed to 5 μmol/L mibefradil (a T-type calcium channel blocker), 10 mmol/L lidocaine and 5 μmoL/L mibefradil + 10 mmol/L lidocaine for 24 h. Cell morphology was examined by electronic microscopy at 24 h of drug exposure. Cell viability (by MTT) and neuronal apoptosis (by flow cytometry) were detected immediately before and at 1, 6, 12 and 24 h of exposure to mibefradil or/and lidocaine.Results In C and M groups, the cells demonstrated dendritic protrusions, enlarged nerve processes and dense lattice. After being exposed to lidocaine for 24 h, the dendritic protrusions disappeared,the cells decreased in size, shrinked and became round; the cell viability was significantly decreased while the neuronal apoptosis increased. The lidocaine-induced changes were significantly attenuated by co-incubation with mibefradil. ConclusionT-type calcium channel is involved in lidocaine-induced neuronal cytotoxicity.     

缺氧／复氧后肾小管上皮细胞ICAM-1表达及Apocynin对其干预作用的研究

目的：研究缺氧/复氧后肾小管上皮细胞氧化应激的变化细胞间黏附分子-1（ICAM-1）蛋白和mRNA的表达及NADPH氧化酶抑制剂Apocynin对其的影响.方法：采用肾小管上皮细胞（HK2）建立缺氧（细胞置于37 ℃、95%N2、5% CO2环境中）/复氧（细胞置于37 ℃、95% O2、5% CO2环境中）细胞模型,设正常对照组,缺氧0.5 h、1 h、2 h/复氧24 h组,及不同浓度（0.05 mmol/L、0.25 mmol/L、0.5 mmol/L）Apocynin干预组.流式细胞术检测细胞内氧化应激水平,逆转录-聚合酶链反应（RT-PCR）法测定细胞ICAM-1 mRNA表达,流式细胞术检测ICAM-1蛋白表达.结果：缺氧/复氧后HK2细胞内氧化应激水平提高,ICAM-1 mRNA和蛋白表达增强,随缺氧时间的延长,细胞内氧化应激水平逐渐升高,ICAM-1mRNA和蛋白表达也逐渐增强 Apocynin呈剂量依赖关系抑制细胞内氧化应激和ICAM-1 mRNA、蛋白表达的上调.结论：缺氧/复氧诱导细胞内氧化应激的产生,诱导ICAM-1表达上调 Apocynin可以通过抑制细胞内氧化应激抑制ICAM-1的上调.     

2015年乳腺癌辅助化疗进展

【摘要】〓乳腺癌是危害我国女性健康的头号杀手,尽管近年来辅助化疗的研究进展突飞猛进,但临床中仍有不少问题未能明确,如辅助化疗的合适人群、化疗的开始时间、蒽环及紫杉类的地位和用法、强化维持治疗的作用、疗效及预后的生物标志物等。本文结合乳腺癌辅助化疗在临床上的常见问题和2015年各大乳腺癌会议阐述乳腺癌辅助化疗的最新进展。     

Alterations in T-Cell Subset Frequency in Peripheral Blood in Obesity

Background: Obesity affects the regulation of immune and inflammatory responses. This study characterizes differences in peripheral blood lymphocyte phenotype in obese humans. Methods: Frequencies of lymphocyte subsets among peripheral blood mononuclear cells were compared between 10 obese (BMI ≥35) and 10 lean subjects, as determined by antibodies directed against cluster differentiation (CD) markers. Results: Obese patients demonstrated an increased frequency of CD3+CD4+ T-cells (mean difference 12%, P=0.004), a decreased frequency of CD3+CD8+ T-cells (mean difference 9.4%, P=0.016) and an increased frequency of CD3+CD8+CD95+ T-cells (mean difference 13.3%, P=0.032). No other differences among T-cell or monocyte subsets were noted. Conclusions: Obesity is associated with alterations in frequencies of peripheral CD4+ and CD8+ T-cells and aberrations in the expression of CD95 among CD8+ T-cells. These data suggest both CD4+ and CD8+ T-cell compartments, as well as the regulation of CD95 expression on CD8+ T-cells, as targets for further study into obesity's effects on the immune system.     

西宁地区烧伤病人动脉血气分析观察

对高海拔地区的27例烧伤病人动脉血气变化进行了分析和观察。结果证明:无论是存活病人还是死亡病人伤后均存在有低氧血症问题。并且在死亡病人和烧伤合并吸入性损伤病人其低氧血症的发生早于单纯烧伤病人。提示:吸入性损伤病人应立即行气管切开术以保障氧气供给,单纯烧伤病人可常规吸氧以维持正常血 PaO_2,ARDS 均发生在合并吸入性损伤的病人,高频喷射通气技术对纠正低氧血症有一定效果。     

Controversies in Fistula in Ano

Managing a complex fistula in ano can be a daunting task for most surgeons; largely due to the two major dreaded complications—recurrence & fecal incontinence. It is important to understand the anatomy of the anal sphincters & the aetiopathological process of the disease to provide better patient care. There are quite a few controversies associated with fistula in ano & its management, which compound the difficulty in treating fistula in ano. This article attempts to clear some of those major controversies.     

β-半乳糖苷酶在体内外成骨细胞中的表达

目的 研究β—半乳糖苷酶(β—gal)在成骨细胞中的表达状况，为阐明MorquioB综合征的发病机制提供依据。方法 裸鼠各器官和骨组织标本行X-gal染色检测。抽取羊和人骨髓行骨髓基质细胞(BMSCs)培养，分为4组：I：Adv-hBMP-2转染组；Ⅱ：Adv—β—gal转染组；Ⅲ：未转染组；Ⅳ：地塞米松诱导组。分别行X-gal染色和RT-PCR检测β—gal的表达。结果 裸鼠骺板两侧、骨膜内面及松质骨的成骨细胞和破骨细胞可见多量β—gal的表达。未转染BMSCs组有少量β—gal的表达，其他3组细胞的β—gal表达增高。结论成骨细胞和破骨细胞可表达多量β—gal，该两种细胞的β—gal缺乏可能是MorquioB综合征骨骼异常的直接原因。     

Fluid-phase transcytosis in the primate epididymis in vitro and in vivo

Ligated tubules from the corpus epididymidis of men and monkeys were incubated in medium containing horseradish peroxidase (HRP) as a marker for fluid-phase endocytosis. HRP was localized by light and electron microscopy after 0, 15, 30 and 60 min of incubation. Movement between the cells was prevented by tight junctions, but bypass of this barrier was apparently achieved by an intracellular vesicular mechanism leading to a time-dependent appearance of HRP in the lumen. Uptake of HRP into basal cells and capture by the lysosomal apparatus of principal cells were also observed. HRP-filled vesicles also appeared in the basal, mid and apical cytoplasm of epithelial cells in the caput 1 h after injection of the tracer into the epididymal circulation of the monkey, suggesting that this pathway also operates in vivo.     

Surgical management of ductal carcinoma in situ in Australia in 1995

Background: In the present paper we describe the presentation and management of ductal carcinoma in situ (DCIS) of the breast in women in Australia in 1995. This representative, national data set provides a historical comparator for studies examining DCIS management that follow. Methods: Surgeons identified by population‐based cancer registries as having treated a new diagnosis of DCIS between 1 April and 30 September 1995 completed a questionnaire on the presentation and management of each case. Results: Two hundred and five surgeons supplied treatment details on 418 DCIS tumours in 415 women . Half of all tumours were detected at BreastScreen clinics and a further 25% were detected at other mammography centres. Twenty‐six percent of tumours were palpable at presentation, 33% were multifocal and 55% were high grade (including comedocarcinoma). Breast conserving therapy (BCT) rather than mastectomy was utilized in 260 (62%) of cases. Tumours that were of low grade, small in size and not multifocal were more likely to be treated by BCT. Surgeons seeing six or more DCIS cases in the 6‐month period were more likely to utilize BCT. Of the conservatively treated cases, 22% were referred for a radiation oncology consultation. The most common reasons for treating DCIS with mastectomy were that the tumour was too extensive or multifocal (63%), it extended to margins of the specimen (42%), or patient concerns about recurrence (34%). Conclusions: In 1995 the majority of DCIS was treated with breast conserving surgery alone. Surgeons treating more DCIS cases were more likely to perform conservative surgery than surgeons treating only one DCIS case in the study period.     

Smoking-Attributable mortality in Spain in 2016

IntroductionSmoking-attributable mortality (SAM) is a valuable indicator that can be used to characterize the course and health burden of the smoking epidemic. The aim of this paper was to estimate SAM in Spain in 2016 in the population aged 35 and over, using the best available evidence.MethodsA smoking prevalence-dependent analysis based on the estimation of population-attributable fractions was performed. Smoking prevalence (never, former, and current smokers) was calculated from a combination of the Spanish Health Survey (2016) and the European Health Survey (2014); the relative risk of death among current and former smokers was taken from the follow-up of various cohorts; and mortality rates were obtained from National Center for Statistics data. SAM estimates are presented globally, and by sex, age groups, and major disease categories: cancer, cardiometabolic diseases and respiratory diseases.ResultsIn 2016, 56,124 deaths were attributed to tobacco consumption, 84% in men (47,000), and 50% in the population aged over 74 (27,795). Overall, 50% of SAM was due to cancer (28,281), 65% of which was lung cancer. One in 4 attributable deaths (13,849) occurred before the age of 65.ConclusionsOne in 7 deaths in Spain in 2016 were attributable to smoking. This estimation of SAM clearly highlights the great impact of smoking on mortality in Spain, mainly due to lung cancer and chronic obstructive pulmonary disease.