黄连素在脊髓损伤中对线粒体的保护作用及机制

目的探讨黄连素对脊髓损伤(SCI)后线粒体氧化损伤的作用和可能机制。方法将36只C57小鼠随机分为假手术组、SCI组(伤后立即腹腔注射10 mg/kg生理盐水)和黄连素组(SCI后立即腹腔注射10 mg/kg黄连素),每组12只。使用PSI-IH脊髓打击器建立小鼠SCI模型,于损伤后24 h处死小鼠,取脊髓组织。使用全自动酶标仪检测各组小鼠脊髓组织线粒体内丙二醛(MDA)、还原型谷胱甘肽(GSH)和超氧化物歧化酶(SOD)的变化;用蛋白质印迹法检测脊髓组织caspase-3、cleaved caspase-3的表达及细胞质内和线粒体内细胞色素C(Cyt C)的表达;用免疫荧光双标染色法检测脊髓组织中神经细胞凋亡情况。结果与假手术组相比,SCI组小鼠脊髓组织线粒体内MDA水平升高,GSH、SOD水平降低;细胞质内Cyt C和脊髓组织中caspase-3、cleaved caspase-3表达水平增高,线粒体内Cyt C表达水平降低;脊髓组织中神经元凋亡比例增高;差异均有统计学意义(P 0.05)。与SCI组相比,黄连素组小鼠脊髓组织线粒体内MDA水平降低,SOD和GSH水平增高;细胞质内Cyt C和脊髓组织中caspase-3、cleaved caspase-3表达水平降低,线粒体内Cyt C表达水平增高;脊髓组织中神经细胞凋亡比例减少;差异均有统计学意义(P 0.05)。结论黄连素可减轻SCI小鼠脊髓组织中神经细胞凋亡,这可能与其抑制线粒体氧化损伤、减少Cyt C释放、降低凋亡蛋白表达有关。     

B淋巴细胞瘤-2蛋白多位点磷酸化在大鼠脊髓损伤后细胞自噬中的表达研究

目的探讨大鼠脊髓损伤(spinal cord injury,SCI)后细胞自噬的变化及其与B淋巴细胞瘤-2(Bcell lymphoma-2,Bcl-2)蛋白多位点磷酸化的关系。方法取40只8周龄雄性SD大鼠,采用改良Allen法制备SCI模型;将造模成功的36只大鼠随机分为SCI组、自噬抑制剂组、自噬促进剂组,每组12只。另取12只大鼠仅切除椎板、不损伤脊髓,作为假手术组。造模结束后,自噬抑制剂组及自噬促进剂组分别于脊髓鞘内注射20μL600 nmol/L 3-甲基腺嘌呤、25 nmol/L雷帕霉素,假手术组及SCI组仅注射20μL生理盐水;每天1次,连续4周。造模后1 d及1、2、4周,采用BBB评分法评价各组大鼠后肢运动功能。末次注射后24 h处死各组大鼠并取脊髓组织,ELISA法检测脊髓组织中过氧化物酶(myeloperoxidase,MPO)活性及TNF-α、IL-1β水平;HE染色观察脊髓组织形态学变化;透射电镜观察脊髓组织中线粒体超微结构变化;免疫荧光染色检测自噬相关蛋白(Beclin1)、微管相关蛋白轻链3(microtubule-associated protein light chain 3,LC3)蛋白表达;TUNEL染色观察脊髓组织神经细胞凋亡;免疫荧光双染检测LC3/TUNEL阳性细胞表达;Western blot检测细胞Bcl-2相关X蛋白(Bcl-2 associated X protein,Bax)、Bcl-2及p-Bcl-2(Ser87)、p-Bcl-2(Ser70)蛋白表达。结果与假手术组相比,SCI组各时间点BBB评分降低,MPO活性、TNF-α、IL-1β水平升高;神经细胞周围间隙增大,细胞肿胀、出现空泡,线粒体中出现自噬小体;Beclin1及LC3蛋白阳性率、神经细胞凋亡率显著升高;LC3、TUNEL阳性细胞增多;Bax、p-Bcl-2(Ser87)、p-Bcl-2(Ser70)蛋白表达升高,Bcl-2蛋白表达降低;以上指标比较差异均有统计学意义(P0.05)。与SCI组相比,自噬抑制剂组各时间点BBB评分降低,MPO活性、TNF-α、IL-1β水平升高;线粒体中出现少量自噬囊泡;Beclin1及LC3蛋白阳性率降低,神经细胞凋亡率显著升高;LC3阳性细胞减少、TUNEL阳性细胞增多;Bax、p-Bcl-2(Ser87)、p-Bcl-2(Ser70)蛋白表达升高,Bcl-2蛋白表达降低。而自噬促进剂组结果与自噬抑制剂组相反;以上指标组间比较差异均有统计学意义(P0.05)。结论大鼠SCI后通过诱导细胞自噬可降低神经细胞凋亡,保护脊髓功能,其机制可能与抑制Bcl-2蛋白多位点磷酸化有关。     

营养剥夺诱导髓核细胞凋亡与BNIP3蛋白表达上调

目的 通过营养剥夺(低氧-无糖-无血清)诱导髓核细胞凋亡,检测髓核细胞线粒体蛋白BNIP3(bcl-2/Adenovirus El B19-kd Protein-Interacting Protein 3)表达。方法 体外分离培养大鼠尾椎间盘髓核细胞,传代至P1代后将细胞分为正常对照组:DMEM/L培养基(1000 mg葡萄糖/L)、10％胎牛血清、21％ O2;实验组:DMEM无糖培养基、无血清、1％ O2;分别将两组细胞培养0、24、48、72 h后,免疫荧光检测BNIP3蛋白表达并定位、流式细胞仪检测细胞凋亡率及线粒体膜电位。结果 免疫荧光检测显示正常对照组细胞低表达BNIP3,定位于胞质且未结合线粒体,实验组显示随培养时间延长,BNIP3表达呈上升趋势,在72 h明显增加,共定位发现BNIP3主要分布于胞质,并与线粒体相结合;流式细胞仪检测发现正常对照组细胞凋亡率为(1.02±0.21)％,实验组细胞凋亡率明显增加(P＜0.05),分别为(4.22±0.34)％、(7.5l±2.33)％、( 19.93±2.58)％,线粒体膜电位结果显示实验组24、48、72 h线粒体膜电位均不同程度降低,分别为(90.23±1.32)％、(87.30±2.21)％、(82.63±2.91)％,均显著低于正常对照组(94.21±3.96)％(P＜0.05)。结论 营养剥夺可能通过诱导BNIP3表达增加并结合线粒体导致髓核细胞凋亡。     

脊神经结扎术后脊髓背角小胶质细胞中miR-195的表达及其对自噬水平的影响

目的 :探讨大鼠脊神经结扎术后脊髓背角小胶质细胞中微核糖核酸-195(micro RNA-195,miR-195)的表达及其对自噬水平的影响与调节机制。方法:32只成年雄性SD大鼠随机分为脊神经结扎组(SNL组)和假手术组(S组),每组16只,SNL组结扎L5段神经制备脊神经结扎模型,造模后1d、3d、5d、10d两组各处死4只大鼠,分离脊髓腰膨大,采用Percoll梯度离心法分离脊髓背角小胶质细胞,Real-time PCR检测两组各时间点脊髓背角小胶质细胞的miR-195表达水平。取12只成年雄性SD大鼠,处死后取脊髓腰膨大,分离脊髓背角小胶质细胞,分为两组,一组采用脂质体法转染miR-195模拟物,另一组加入转染试剂,检测两组小胶质细胞自噬体膜标记蛋白轻链3(light chain 3,LC3)的表达水平;再取小胶质细胞分为三组,分别将含有野生型及突变型自噬相关基因14(ATG14)3′非编码区(3′UTR)的报告基因质粒、p RL-TK质粒miR-195模拟物和对照转入HEK 293细胞培养48h,荧光显微镜下观察miR-195的直接作用靶点,并检测三组ATG14蛋白的表达。取24只健康SD大鼠脊髓腰膨大,分离脊髓背角小胶质细胞,分为三组分别转染miR-195模拟物、抑制物和转染试剂,培养48h,采用免疫蛋白印记(Western blot)法检测三组ATG14蛋白的表达水平;再取小胶质细胞分为三组,分别转染pEGFP-LC3、pEGFP-LC3+miR-195模拟物及pEGFP-LC3+miR-195模拟物+pCMV-ATG14培养48h,染色后荧光显微下观察自噬斑点数量。结果 :SNL组各时间点大鼠脊髓背角小胶质细胞中miR-195表达均明显上调,与同时间点S组比较均有显著性差异(P0.05)。转染miR-195模拟物后,LC3的表达水平(0.61±0.07)较对照组(1.21±0.08)显著性降低(P0.05)。转入野生型ATG14 3′UTR的报告基因质粒的HEK 293细胞的荧光强度较对照显著性减弱(0.65±0.04 vs 1.01±0.01,P0.05),突变型与对照无显著性变化(0.99±0.03 vs1.00±0.02,P0.05)。转染miR-195模拟物后小胶质细胞中ATG14的表达显著性降低(P0.05);转染miR-195抑制物后ATG14的表达显著性升高(P0.05)。转染pEGFP-LC3与pEGFP-LC3+miR-195模拟物较转染pEGFP-LC3+miR-195模拟物+pCMV-ATG14时自噬数量降低(P0.05)。结论 :miR-195在大鼠脊神经结扎模型脊髓背角小胶质细胞中高表达,降低自噬蛋白LC3表达;ATG14蛋白受miR-195负调控,miR-195可能通过降低ATG14的表达抑制小胶质细胞自噬。     

白介素-1受体拮抗剂对大鼠急性脊髓损伤后神经细胞凋亡和caspase-3表达的影响

目的：观察白介素-1受体拮抗剂（IL—1Ra）对脊髓损伤（SCI）后继发性神经细胞凋亡和caspase-3表达的影响。方法：60只SD大鼠，随机分为假手术组、脊髓损伤组、IL-1Ra治疗组和生理盐水对照组，每组15只。采用Allen’s法建立大鼠急性SCI动物模型．IL—1Ra治疗组和生理盐水对照组于SCI后立即硬膜下腔内分别注射IL-1Ra（10μg／10μl）和等量生理盐水，于伤后24h以损伤为中心（假手术组取相应部位），切取长约8mm脊髓组织．用蛋白印迹法和免疫组化染色法检测caspase-3表达的变化：采用实时定量PCR法检测caspase-3mRNA的表达情况；用原位末端标记法（TUNEL）检测SCI后神经细胞凋亡情况。结果：SCI后24h，SCI组与假手术组比较受损伤的脊髓组织中caspase-3mRNA和蛋白表达水平均显著升高（P〈O．05），且TUNEL阳性细胞明显增多（P〈O．01）：IL—1Ra治疗组大鼠受损伤节段脊髓组织caspase-3表达及TUNEL阳性细胞数较生理盐水对照组）均明显减少（P〈O．01）。结论：IL-1Ra治疗可减少急性SCI后脊髓组织中caspase-3的表达和神经细胞凋亡的发生。     

BNIP3与LC3B在椎间盘退行性变过程中的作用

目的研究BCL2/腺病毒E1B19k Da相互作用蛋白3(BNIP3)基因及微管相关蛋白轻链3B(LC3B)基因在退变椎间盘中的表达情况,探讨其与椎间盘退行性变分级之间的相关性。方法收集2016年4月—2016年7月因腰椎椎间盘突出症于本院接受手术治疗的21例患者的退变腰椎椎间盘标本25个,依据Pfirrmann分级分成5组,分别采用实时荧光定量PCR技术和蛋白质印迹法检测BNIP3、LC3B的m RNA和蛋白表达量,用实时荧光定量PCR技术检测Bcl-2、Bax、Caspase-3的mRNA表达量,并分析BNIP3表达量、LC3B表达量、细胞自噬、细胞凋亡与Pfirrmann分级之间的关系。结果退变椎间盘组织中BNIP3、LC3B在mRNA和蛋白水平的表达均随椎间盘退行性变程度加重而减少。Bcl-2 m RNA的表达随椎间盘退行性变程度加重而减少,Bax与Casepase-3 mRNA的表达随椎间盘退行性变程度加重而增多。结论随着椎间盘退行性变程度的加重,BNIP3与LC3B的表达减少,组织内细胞凋亡水平升高,细胞自噬对组织的保护作用逐渐下降。提示BNIP3与LC3B在腰椎椎间盘退行性变过程中具有重要的调节作用,可能是细胞自噬和凋亡之间的桥梁蛋白。     

七氟醚预处理对大鼠脊髓缺血再灌注损伤的影响及自噬在其中的作用

目的 评价七氟醚预处理对大鼠脊髓缺血再灌注损伤的影响及自噬在其中的作用.方法 成年雄性SD大鼠45只,体重420～450 g,采用随机数字表法分为5组(n=9):对照组(Con组)、脊髓缺血再灌注组(I/R组)、七氟醚预处理组(Sevo组)、特异性自噬抑制剂3-甲基腺嘌呤组(3-MA组)和3-MA+七氟醚预处理组(3-MA+ Sevo组).I/R组胸主动脉球囊阻断+体循环低血压制备大鼠脊髓缺血再灌注模型,Sevo组于缺血前24h时吸入3.4％七氟醚2h,3-MA组和3-MA+ Sevo组分别于再灌注即刻和吸入七氟醚前15 min时鞘内注射20出3-MA(10 mmol/L).于再灌注24h时采用神经功能缺陷评分(NDS评分)法评价大鼠神经功能,随后处死取脊髓,Western blot法检测LC3B、Beclin 1、Bcl-2蛋白的表达水平.结果 与Con组比较,I/R组脊髓LC3B、Beclin 1蛋白表达上调,Bcl-2蛋白表达下调,NDS评分升高(P＜0.05);与I/R组比较,Sevo组、3-MA组和3-MA+ Sevo组脊髓LC3B、Beclin 1蛋白表达下调,Bcl-2蛋白表达上调,NDS评分降低(P＜0.05);Sevo组、3-MA组和3-MA+ Sevo组各指标比较差异无统计学意义(P＞0.05).结论 七氟醚预处理可减轻大鼠脊髓缺血再灌注损伤,其机制可能与上调Bcl-2,抑制自噬溶酶体途径,减轻自噬有关.     

抑制自噬对5-氟尿嘧啶治疗肝癌疗效的影响及机制研究

目的研究自噬特异性抑制剂3-甲基腺嘌呤（3-MA）对5-氟尿嘧啶（5-FU）诱导肝癌细胞系SMMC7721凋亡的影响,并初步探讨其机制。方法利用单丹（磺）酰戊二胺（MDC）染色技术,在荧光显微镜下对细胞自噬进行定性观察;以CCK8法检测3-MA抑制细胞自噬前后经5-FU诱导SMMC7721细胞的存活,凋亡以AnnexinⅤ/PI流式细胞分析法检测;以Western blot法分别检测自噬特异性蛋白LC3及凋亡蛋白caspase-3活化片段和PARP裂解片段的表达。结果 5-FU处理肝癌SMMC7721细胞48 h后,可诱导其发生自噬,细胞存活率为（60.73±2.65）%,凋亡率为（40.42±2.34）%;联合应用3-MA处理48 h后,可使肝癌SMMC7721细胞存活率明显降低（P〈0.01）,为（42.31±1.32）%,而细胞凋亡率显著增加（P〈0.01）,为（60.92±2.99）%,同时引起自噬特异性蛋白LC3-Ⅱ及凋亡蛋白caspase-3活化片段和PARP裂解片段表达增加,其灰度值比较差异均有统计学意义（均P〈0.01）。结论自噬在5-FU诱导肝癌细胞系SMMC7721凋亡过程中起保护性作用,抑制自噬可提高肝癌SMMC7721细胞对5-FU的敏感性,其可能主要通过激活caspase-3及剪切PARP来实现的。因此,自噬特异性抑制剂3-MA可能为提高肝癌对5-FU的敏感性提供新思路。     

营养剥夺诱导髓核细胞Bcl-2/腺病毒干扰蛋白3表达及线粒体转位的实验研究

目的通过营养剥夺模拟体内髓核细胞退变微环境,检测Bcl-2/腺病毒干扰蛋白3（Bcl-2/adenovirusE1B 19-kDa-interacting protein 3,BNIP3）表达及线粒体转位情况,为进一步探索髓核细胞退变死亡机制提供实验依据。方法成年清洁级SD大鼠2只,雌雄不限,体重150～200 g。体外分离获取鼠尾椎问盘髓核细胞,将传代后细胞分别置入正常环境（对照组:L-DMEM培养基、10%FBS、21%O₂）和营养剥夺环境（实验组:DMEM无糖无血清培养基、1%O₂）培养24、48、72 h后,实时荧光定量PCR、细胞免疫荧光染色及Western blot检测BNIP3基因及蛋白表达,流式细胞仪检测凋亡率及线粒体膜电位。结果实时荧光定量PCR、细胞免疫荧光染色及Western blot检测显示对照组细胞低表达BNIP3;实验组随培养时间延长,BNIP3表达呈上升趋势,且BNIP3与线粒体相结合;除培养后24 h实验组BNIP3基因表达与对照组比较差异无统计学意义（P>0.05）外,其余各时间点实验组BNIP3基因及蛋白表达与对照组比较差异均有统计学意义（P<0.05）。流式细胞仪检测显示,对照组细胞凋亡率较低,且细胞保持较高的线粒体膜电位;而实验组随培养时间延长细胞凋亡率增加、线粒体膜电位降低,与对照组比较差异均有统计学意义（P<0.05）。结论营养剥夺可能通过诱导BNIP3表达增加并结合线粒体导致线粒体功能障碍,最终导致髓核细胞死亡。     

甲基强的松龙对大鼠脊髓损伤后神经细胞凋亡的影响及其机理

目的研究甲基强的松龙(MP)对大鼠横断性脊髓损伤(SCI)后神经细胞凋亡的影响及其作用机理.方法60只成年Wistar大鼠随机分成正常对照组、脊髓损伤组和MP治疗组,每组20只,MP治疗组在横断T10脊髓组织后30min经尾静脉给予MP治疗,损伤组和对照组未予任何治疗.MP治疗组和脊髓损伤组大鼠于脊髓损伤后8h、24h、3d和1周取材,采用透射电镜、TUNEL染色观察细胞凋亡情况,采用免疫组织化学染色观察Fas、半胱氨酸蛋白酶(caspase)-8和caspase-3在SCI前后的变化情况,采用改良Tarlov评分方法观察大鼠后肢运动功能.结果SCI后24h大鼠后肢运动功能逐渐恢复,MP治疗组大鼠的后肢运动功能恢复优于损伤组,7d后尤其明显.TUNEL染色和电镜检查证实SCI后8h即有凋亡细胞出现,其中既有神经元也有胶质细胞3d凋亡细胞数达到高峰;7d仍有凋亡细胞存在,但已明显减少;各时间点治疗组凋亡细胞数量明显少于损伤组(P＜0.05).治疗组和损伤组在SCI后8h可以检测到少量的Fas和caspase-8阳性神经元及胶质细胞,Fas和caspase-8的表达在SCI后3d达到高峰,7d表达下降,各时间点治疗组的Fas和caspase-8灰度值明显大于损伤组,二者有显著性差异(P＜0.05).治疗组和损伤组caspase-3的表达在SCI后8h均逐渐增加(与对照组相比),7d达到高峰,治疗组灰度值大于损伤组,但二者无显著性差异.结论MP能抑制大鼠脊髓横断性脊髓损伤后的神经细胞凋亡,但不能推迟细胞凋亡出现的高峰时间;MP抑制细胞凋亡的途径可能通过非特异性抑制Fas和caspase-8的表达来实现.     

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.