苯乙双胍联合己糖激酶抑制剂诱导三阴性乳腺癌细胞凋亡

目的 探讨降糖药物苯乙双胍联合己糖激酶抑制剂2-脱氧葡萄糖（2-DG）对三阴性乳腺癌细胞4T1和MDA-MB-231凋亡作用的影响。方法 苯乙双胍单独或联合2-DG处理4T1与MDA-MB-231细胞48 h,用SRB法检测细胞的增殖,流式细胞术检测细胞凋亡,试剂盒检测培养上清液中葡萄糖消耗量和乳酸含量,多功能化学发光仪检测线粒体呼吸链复合物I活性,海马能量检测仪测定细胞线粒体耗氧量(OCR)。结果 苯乙双胍组的4T1与MDA-MB-231细胞上清液己糖激酶表达量（4.6±0.17,3.73±0.21）,葡萄糖消耗量（356±31,397±42）μg/10⁵个细胞,乳酸浓度（5.59±0.52,7.83±0.78）μmol/L均高于空白组的已糖激酶表达量（1±0.15,1±0.12）,葡萄糖消耗量（289±25,301±32）μg/10⁵个细胞,乳酸浓度（2.37±0.18,4.01±0.45）μmol/L（P < 0.01）;苯乙双胍联用2-DG组的细胞存活率（64.63±2.28,51.97±2.29）% ,即使降低90%剂量,仍高于苯乙双胍组（86.70±1.83,85.53±1.46）%（P<0.001）,两药联用极大地促进了4T1与MDA-MB-231细胞的凋亡,此外,相比于苯乙双胍组（5.59±0.52,7.83±0.78）μmol/L,苯乙双胍与2-DG联用组（3.46±0.37,5.18±0.62）μmol/L细胞的乳酸产量也大大下降（P<0.01）;与苯乙双胍或2-DG单药组相比,苯乙双胍联合2-DG组可显著抑制荷瘤小鼠体内肿瘤的生长速度（P<0.01）;苯乙双胍联合2-DG组荷瘤小鼠中位生存时间72.5 d,高于苯乙双胍组57 d、2-DG组55.5 d（P<0.01）,苯乙双胍联合2-DG可以延长荷瘤小鼠生存时间。结论 己糖激酶抑制剂2-DG显著增强了苯乙双胍对三阴性乳腺癌细胞的治疗作用。     

藏红花素联合顺铂对人宫颈癌HeLa细胞协同抑制作用的研究

目的 探索藏红花素联合顺铂对人宫颈癌HeLa细胞的协同抑制作用及相关调控机制。方法 取对数生长期人宫颈癌HeLa细胞,设置空白对照组（DMSO）、藏红花素组（400 μg·mL^-1）、顺铂组（5 μg·mL^-1）、联合组（藏红花素400 μg·mL^-1+顺铂5 μg·mL^-1）。干预48 h后,CCK-8检测HeLa细胞增殖抑制率,采用CompuSyn软件计算藏红花素与顺铂的联合指数（CI）,Annexin V-FITC染色法检测细胞凋亡,流式细胞术检测细胞周期分布,Western blotting检测激活型半胱氨酸天冬氨酸蛋白酶-3（Cleaved Caspase-3）、B细胞淋巴瘤/白血病-2（Bcl-2）、Bcl-2相关X蛋白（Bax）、细胞周期素D1（Cyclin D1）、周期蛋白依赖激酶2（CDK2）的表达。结果 与顺铂组比较,联合组细胞增殖抑制率显著升高（P<0.05）,CI为0.68,具有中度协同效应;细胞凋亡率显著升高（P<0.01）,G₀/G₁期细胞比例显著升高（P<0.05）,而G₂/M期比例显著降低（P<0.01）,Cleaved Caspase-3、Bax蛋白表达水平及Bax/Bcl-2比值均显著升高（P<0.05）,Cyclin D1、CDK2蛋白表达水平显著降低（P<0.01）。与空白对照组比较,藏红花素组G₀/G₁期细胞比例显著升高而G₂/M期比例显著降低（P<0.01）,Cleaved Caspase-3、Bax表达水平及Bax/Bcl-2比值均显著升高（P<0.01）,Cyclin D1、CDK2表达水平显著降低（P<0.05）。结论 藏红花素联合顺铂可协同抑制人宫颈癌HeLa细胞的增殖和生长,其作用机制可能与调控凋亡相关蛋白的表达从而促进细胞凋亡、阻滞细胞周期进程有关。     

瑞香素对三阴性乳腺癌细胞株MDA-MB-231的抑制作用及其机制研究

目的 探讨瑞香素对三阴性乳腺癌细胞株MDA-MB-231的增殖、迁移及侵袭的抑制作用及其潜在机制。方法 体外培养MDA-MB-231细胞，随机分为对照组和瑞香素10，20，40 μg·mL^–1组。以MTT法检测细胞的增殖情况；通过克隆形成试验检测各组MDA-MB-231细胞克隆形成情况；划痕试验及Transwell观测细胞迁移和侵袭情况；Western blotting检测Vimentin、MMP9、Cyclin D1、CDK4蛋白表达量。结果 与对照组相比，瑞香素组（10，20，40 μg·mL^–1）显著抑制细胞增殖（P<0.05或P<0.01）；瑞香素组（10，20，40 μg·mL^–1）可以抑制人乳腺癌细胞株MDA-MB-231的克隆形成（P<0.01）；瑞香素组（20，40 μg·mL^–1）细胞的迁移能力和侵袭能力显著下降（P<0.01）；瑞香素组（20，40 μg·mL^–1）细胞Vimentin、MMP9、Cyclin D1、CDK4蛋白表达量显著降低（P<0.01）。结论 瑞香素可以抑制三阴性乳腺癌细胞株MDA-MB-231的增殖、迁移及侵袭能力，其作用机制可能与下调Vimentin、MMP9、Cyclin D1、CDK4的表达有关。     

槐耳颗粒联合DC-CIK细胞对乳腺癌MDA-MB-231干细胞体内外杀伤作用研究

目的 探究白屈菜红碱（CHE）对腺样囊性癌细胞（ACC2）生长的抑制作用及机制。方法 利用CCK8法、EdU法、Hoechst33342/PI双染色法、试剂盒法检测CHE对ACC2细胞活力、细胞增殖、细胞凋亡和活性氧（ROS）水平的影响;通过Western blotting技术检测CHE对Cleaved-Caspase 3、PARP、NF-κB、p-JNK、p-p38蛋白表达的影响;利用斑马鱼移植瘤模型检测CHE对斑马鱼体内ACC2细胞生长的抑制作用。结果 CCK-8结果显示：与对照组比较,2、3、4、5、6、7、8、9、10 μmol/L的CHE显著降低ACC2细胞的存活率（P<0.05、0.01）,且呈浓度相关性; ROS检测结果显示：与对照组比较,5、8 μmol/L的CHE导致ACC2细胞内的ROS水平显著上升（P<0.05、0.01）; EdU增殖检测结果表明：与对照组比较,5、8 μmol/L的CHE致使ACC2细胞的增殖能力显著下降（P<0.01）;Hoechst/PI染色结果显示：与对照组比较,CHE 5、8 μmol/L组ACC2细胞凋亡率显著上升（P<0.01）。抗氧化剂N-乙酰半胱氨酸（NAC）显著抑制CHE诱导的ROS水平升高、细胞凋亡增加（P<0.01）;Western blotting结果显示：2、5、8 μmol/L的CHE能够显著上调Cleaved-Caspase 3、PARP、NF-κB蛋白的表达（P<0.01）,且呈现浓度相关性,5、8 μmol/L的CHE能够显著上调p-JNK的蛋白表达（P<0.01）,8 μmol/L的CHE能够显著上调p-p38的蛋白表达（P<0.01）;NAC显著降低由CHE导致的Cleaved-Caspase 3、PARP、NF-κB、p-JNK、p-p38蛋白表达增加（P<0.01）,5、8 μmol/L CHE能够有效抑制斑马鱼体内肿瘤的生长（P<0.01）。结论 体外及斑马鱼移植瘤模型证明,CHE可以有效抑制ACC2细胞生长,其机制与提高细胞ROS水平,上调NF-κB、p-JNK、p-p38表达,从而抑制细胞增殖、诱导细胞凋亡相关。     

miR-10b-5p通过靶向SUFU介导乳腺癌细胞对放疗的敏感性★

目的 探讨miR-10b-5p在乳腺癌细胞放疗敏感性中的作用及相关机制。方法 采用qPCR和Western blotting检测正常乳腺细胞MCF-10A和乳腺癌细胞MCF-7、SKBR-3、MDA-MB-231中miR-10b-5p mRNA、SUFU mRNA和蛋白的表达。在MDA-MB-231细胞中转染miR-10b-5p inhibitor对miR-10b-5p进行敲减，6 Gy ⁶⁰Co γ-射线照射2 h，分别采用克隆形成实验和流式细胞术检测细胞的增殖和凋亡水平；双荧光素酶报告实验验证靶基因SUFU，回补实验验证miR-10b-5p是否通过靶向SUFU介导乳腺癌细胞对放疗的敏感性。结果 3种乳腺癌细胞系中miR-10b-5p的表达均显著高于正常乳腺细胞MCF-10A（P<0.05）。与miR-NC组相比，miR-10b-5p inhibitor组细胞增殖水平明显下降（P<0.05），凋亡水平显著上升（P<0.05）。敲减miR-10b-5p可增加野生型SUFU 3''UTR的荧光强度（P<0.05），而对突变型SUFU 3''UTR的荧光强度无明显影响（P>0.05）。此外，miR-10b-5p inhibitor组SUFU蛋白表达水平显著高于miR-NC组（P<0.05）。与miR-NC+si-NC组相比，miR-10b-5p inhibitor+si-NC组细胞增殖水平显著降低（P<0.05），miR-10b-5p inhibitor+si-SUFU#2组细胞增殖水平明显回升，且高于miR-10b-5p inhibitor+si-NC组（P<0.05）。结论 乳腺癌细胞中miR-10b-5p呈高表达，敲减miR-10b-5p可增强乳腺癌细胞对放疗的敏感性，其机制可能与靶向抑制SUFU相关。     

大黄素诱导人肝癌HepG2细胞线粒体凋亡作用研究

目的 研究大黄素对人肝癌HepG2细胞线粒体凋亡的影响。方法 培养人肝癌HepG2细胞,与5、10、20、40、60、80、100 μmol/L的大黄素作用24、48 h,MTS法检测细胞增殖;40、80、160 μmol/L大黄素作用HepG2细胞24 h,AO/EB双荧光染色法观察细胞凋亡的形态学改变;Annexin V/PI染色经流式细胞仪检测细胞凋亡;分光光度法检测caspase 3活性;ATP试剂盒检测细胞ATP含量,不同荧光探针加载后流式细胞仪测定大黄素对HepG2细胞内活性氧（ROS）含量、Ca²⁺浓度、线粒体膜电位（MMP）变化的影响。结果 大黄素抑制HepG2细胞生长,且呈时间、浓度相关性,半数抑制浓度（IC₅₀）为（77.42±1.25）μmol/L;随着大黄素浓度升高,AO/EB双染观察到细胞核浓缩、碎裂、凋亡小体等凋亡形态;与对照组比较,大黄素40、80、160 μmol/L作用于HepG2细胞24 h后细胞凋亡率显著增加,caspase 3活性显著增强,ROS水平、Ca²⁺浓度明显增加（P<0.05、0.01、0.001）,80、160 μmol/L组线粒体膜电位明显降低,ATP含量显著下降（P<0.05、0.01、0.001）。结论 大黄素造成HepG2细胞内ROS堆积,ATP合成功能障碍,线粒体膜电位明显下降,进而诱导线粒体通透转运孔开放,导致钙离子和细胞色素C外流,活化caspase蛋白家族,导致细胞凋亡。     

尿石素A对乳腺癌细胞MCF-7增殖、凋亡的影响及其机制研究

目的 研究尿石素A对乳腺癌细胞MCF-7增殖、凋亡的影响并探讨其作用机制。方法 CCK-8法考察不同浓度尿石素A作用12、24、36、48 h对MCF-7细胞增殖能力的影响;细胞凋亡染色法考察20、40 μmol/L的尿石素A对MCF-7细胞凋亡的影响;实时荧光定量PCR（RT-qPCR）检测c-Myc、Cyclin D1、Bcl-2、Bax mRNA的表达水平;Western blotting法检测c-Myc、Cyclin D1、Bcl-2、Bax蛋白的表达水平。结果 尿石素A对MCF-7细胞增殖具有抑制作用且呈时间浓度相关性;细胞凋亡染色显示,20、40 μmol/L尿石素A给药后均能够诱导MCF-7细胞凋亡;RT-qPCR及Western blotting结果显示,20、40 μmol/L尿石素A能够显著降低MCF-7细胞中c-Myc、Cyclin D1、Bcl-2 mRNA及蛋白的表达水平（P<0.05、0.01）,升高Bax mRNA及蛋白的表达水平（P<0.05、0.01）。结论 尿石素A具有抑制MCF-7细胞增殖并诱导其凋亡的作用,其作用机制可能与抑制c-Myc、Cyclin D1、Bcl-2表达,升高Bax表达水平有关。     

一测多评法测定安神宁中4个木脂素含量

目的 建立测定安神宁中4个木脂素含量的一测多评方法(QAMS)。方法 采用高效液相色谱（HPLC）外标法,同时测定安神宁中五味子醇甲、五味子醇乙、五味子甲素、五味子乙素含量,并以五味子醇甲为内参物,建立一测多评法同时测定四个成分含量。结果 五味子醇甲、五味子醇乙、五味子甲素、五味子乙素分别在0.020 7～1.657 6 μg（r=0.999 9）、0.009 8～0.784 6 μg（r=0.999 9）、0.008 2～0.652 2 μg（r=0.999 9）、0.008 1～0.645 8 μg（r=0.999 9）范围内线性关系良好,平均回收率为98.52%、103.43%、109.69%、107.92%,校正因子重现性良好,校正因子法与外标法测定值之间无显著差异。结论 该方法准确、可靠,重复性好,一测多评法可用于安神宁的质量控制。     

来氟米特通过调节miR-449a在肺纤维化中的机制研究

目的 探究来氟米特（leflunomide,LEF）通过调节微小RNA（microRNA,miR）-449a在肺纤维化中的机制研究。方法 将人肺成纤维细胞MRC-5分为6组,即对照组、LEF组、LEF+mimic组、mimic组、LEF+inhibitor组和inhibitor组。通过质粒转染miR-449a mimic或inhibitor来过表达或沉默miR-449a,在5 mg/L LEF的条件下培养48 h。分别通过CCK-8法、克隆形成实验和流式细胞术检测各组细胞活力、细胞增殖能力和凋亡率。使用免疫荧光染色检测α平滑肌肌动蛋白（α smooth muscle actin,α-SMA）胶质蛋白I（collagen I,col I）。分别使用qPCR和Western blot检测miRNA和蛋白的水平。结果 mimic组miR-449a水平显著高于对照组（P<0.05）。LEF组和inhibitor组的miR-449a水平显著低于对照组（P<0.05）。LEF+mimic组的miR-449a的表达水平显著高于LEF组,LEF+inhibitor组的miR-449a水平显著低于LEF组（P<0.05）。LEF组和inhibitor组的细胞活力和细胞增殖能力显著高于对照组（P<0.05）。mimic组的细胞活力和细胞增殖能力显著低于对照组（P<0.05）。LEF+mimic组的细胞活力和细胞增殖能力显著低于LEF组而LEF+inhibitor组的细胞活力显著高于LEF组（P<0.05）。LEF组和inhibitor组的细胞凋亡率低于对照组（P<0.05）,mimic组的细胞凋亡率显著高于对照组（P<0.05）。LEF+mimic组的细胞凋亡率显著高于LEF组而LEF+inhibitor组的凋亡率显著低于LEF组（P<0.05）。LEF组和inhibitor组的α-SMA和Col I蛋白的荧光强度显著高于对照组（P<0.05）,mimic组的相对荧光强度低于对照组（P<0.05）。LEF+mimic组的α-SMA和Col I蛋白相对荧光强度显著低于LEF组,LEF+inhibitor组的α-SMA和Col I蛋白相对荧光强度显著高于LEF组（P<0.05）。LEF组和inhibitor组的p-JNK/JNK水平高于对照组（P<0.05）,mimic组的p-JNK/JNK水平显著低于对照组（P<0.05）,LEF+mimic组中p-JNK/JNK水平显著低于LEF组而LEF+inhibitor组的p-JNK/JNK水平显著高于LEF组（P<0.05）。结论 LEF可能通过抑制肺成纤维细胞中miR-449a的表达激活JNK途径,从而诱导成纤维细胞的活化和增殖,抑制其凋亡,从而引起肺纤维化。     

沉默CDK7通过下调YAP表达诱导子宫内膜癌细胞凋亡

目的 研究沉默细胞周期蛋白依赖性激酶7（CDK7）诱导Yes相关蛋白（YAP）表达下调对子宫内膜癌HEC-1-A细胞凋亡的影响。方法 利用siRNA干扰技术沉默HEC-1-A细胞中CDK7的表达，采用qPCR和Western blotting检测siRNA干扰后CDK7的表达水平，CCK-8实验检测沉默CDK7对HEC-1-A细胞活力的影响，流式细胞术检测沉默CDK7对HEC-1-A细胞凋亡的影响，Western blotting检测沉默CDK7对YAP和磷酸化YAP蛋白及其下游蛋白Cyr16、CTGF表达的影响，凋亡实验检测共转染si-CDK7和pcDNA3.1-YAP对细胞凋亡的影响。结果 转染si-CDK7后，HEC-1-A细胞中CDK7 mRNA和蛋白表达水平均显著下降（P<0.01），细胞活性显著降低（P<0.01），细胞凋亡率显著升高（P<0.01），YAP和磷酸化YAP蛋白及其下游蛋白Cyr16、CTGF表达水平明显下降（P<0.01）；共转染pcDNA3.1-YAP可逆转沉默CDK7导致的细胞凋亡（P<0.01）。结论 沉默CDK7可诱导YAP蛋白表达下调，促进子宫内膜癌HEC-1-A细胞凋亡。     

Synthesis,Cytotoxicity and Antileishmanial Activity of Some N-(2-(indol-3-yl)ethyl)-7-chloroquinolin-4-amines

We report herein the condensation of 4,7-dichloroquinoline (1) with tryptamine (2) and D-tryptophan methyl ester (3) . Hydrolysis of the methyl ester adduct (5) yielded the free acid (6) . The compounds were evaluated in vitro for activity against four different species of Leishmania promastigote forms and for cytotoxic activity against Kb and Vero cells. Compound (5) showed good activity against the Leishmania species tested, while all three compounds displayed moderate activity in both Kb and Vero cells.     

Efficacy of gut lavage,hemodialysis, and hemoperfusion in the therapy of paraquat or diquat intoxication

Clinical and in vitro investigations were carried out to test the efficacy of gut lavage, hemodialysis, and hemoperfusion in the treatment of poisoning with paraquat or diquat. In a patient suffering from diquat intoxication 130 times more diquat was removed by gut lavage 30 h after ingestion than was removed by complete aspiration of the gastric contents.Determination of in vitro clearances for paraquat and diquat by hemodialysis showed that, at serum concentrations of 1–2 ppm, such as are frequently encountered in poisoning in man, toxicologically relevant quantities of herbicide cannot be removed from the body. At a concentration of 20 ppm, on the other hand, hemodialysis proved to be effective, the clearance being 70 ml/min at a blood flow rate of 100 ml/min. The efficacy of hemoperfusion with coated activated charcoal was on the whole better. Especially at concentrations around 1–2 ppm, the clearance values for hemoperfusion were some 5–7 times higher than those for hemodialysis.In a patient suffering from paraquat poisoning, both hemodialysis as well as hemoperfusion were carried out. The in vitro results could be confirmed: At serum concentrations of paraquat less than 1 ppm no clearance could be obtained by hemodialysis while by hemoperfusion with activated charcoal quite high clearance values were measured and the serum level dropped down to zero.

---

Zusammenfassung Klinische Untersuchungen und Laboratoriumsversuche wurden durchgeführt, um die Wirksamkeit von Darmspülung, Hämodialyse und Hämoperfusion bei Paraquat- und Deiquat-Vergiftungen zu prüfen.Bei einem Patienten wurde 30 Std nach Deiquat-Aufnahme durch Darmspülung 130mal mehr Deiquat entfernt als durch vollständige Aspiration des Mageninhaltes. In vitro-Versuche ergaben, daß bei Blutserumkonzentrationen von 1–2 ppm, die bei Vergiftungen oft gemessen werden, durch Hämodialyse keine toxikologisch relevanten Paraquat- oder Deiquat-Mengen entfernt werden können. Dagegen erwies sich die Hämodialyse bei 20 ppm und einer Blutumlaufgeschwindigkeit von 100 ml/min mit einer Clearance von 70 ml/min als wirksam. Die Hämoperfusion mit beschicheter Aktivkohle war in diesen Versuchen aber eindeutig überlegen, denn insbesondere bei Konzentrationen um 1–2 ppm waren die Clearance-Werte 5–7mal höher als bei der Hämodialyse.Die in vitro-Ergebnisse wurden bei einem Patienten mit einer Paraquat-Vergiftung bestätigt: Bei Konzentrationen unter 1 ppm war die Hämodialyse wirkungslos, während durch Hämoperfusion relativ hohe Clearance-Werte erreicht wurden, so daß der Serumspiegel rasch unter die Nachweisgrenze abfiel.

     

In vitro studies on sterically stabilized liposomes (SL) as enzyme carriers in organophosphorus (OP) antagonism

This study describes a new approach for organophosphorous (OP) antidotal treatment by encapsulating an OP hydrolyzing enzyme, OPA anhydrolase (OPAA), within sterically stabilized liposomes. The recombinant OPAA enzyme was derived from Alteromonas strain JD6. It has broad substrate specificity to a wide range of OP compounds: DFP and the nerve agents, soman and sarin. Liposomes encapsulating OPAA (SL)* were made by mechanical dispersion method. Hydrolysis of DFP by (SL)* was measured by following an increase of fluoride ion concentration using a fluoride ion selective electrode. OPAA entrapped in the carrier liposomes rapidly hydrolyze DFP, with the rate of DFP hydrolysis directly proportional to the amount of (SL)* added to the solution. Liposomal carriers containing no enzyme did not hydrolyze DFP. The reaction was linear and the rate of hydrolysis was first order in the substrate. This enzyme carrier system serves as a biodegradable protective environment for the recombinant OP-metabolizing enzyme, OPAA, resulting in prolongation of enzymatic concentration in the body. These studies suggest that the protection of OP intoxication can be strikingly enhanced by adding OPAA encapsulated within (SL)* to pralidoxime and atropine.     

Lung disease and PKCs

The lung offers a rich opportunity for development of therapeutic strategies focused on isozymes of protein kinase C (PKCs). PKCs are important in many cellular responses in the lung, and existing therapies for pulmonary disorders are inadequate. The lung poses unique challenges as it interfaces with air and blood, contains a pulmonary and systemic circulation, and consists of many cell types. Key structures are bronchial and pulmonary vessels, branching airways, and distal air sacs defined by alveolar walls containing capillaries and interstitial space. The cellular composition of each vessel, airway, and alveolar wall is heterogeneous. Injurious environmental stimuli signal through PKCs and cause a variety of disorders. Edema formation and pulmonary hypertension (PHTN) result from derangements in endothelial, smooth muscle (SM), and/or adventitial fibroblast cell phenotype. Asthma, chronic obstructive pulmonary disease (COPD), and lung cancer are characterized by distinctive pathological changes in airway epithelial, SM, and mucous-generating cells. Acute and chronic pneumonitis and fibrosis occur in the alveolar space and interstitium with type 2 pneumocytes and interstitial fibroblasts/myofibroblasts playing a prominent role. At each site, inflammatory, immune, and vascular progenitor cells contribute to the injury and repair process. Many strategies have been used to investigate PKCs in lung injury. Isolated organ preparations and whole animal studies are powerful approaches especially when genetically engineered mice are used. More analysis of PKC isozymes in normal and diseased human lung tissue and cells is needed to complement this work. Since opposing or counter-regulatory effects of selected PKCs in the same cell or tissue have been found, it may be desirable to target more than one PKC isozyme and potentially in different directions. Because multiple signaling pathways contribute to the key cellular responses important in lung biology, therapeutic strategies targeting PKCs may be more effective if combined with inhibitors of other pathways for additive or synergistic effect. Mechanisms that regulate PKC activity, including phosphorylation and interaction with isozyme-specific binding proteins, are also potential therapeutic targets. Key isotypes of PKC involved in lung pathophysiology are summarized and current and evolving therapeutic approaches to target them are identified.     

Steroidal sapogenin contents in some domestic plants

In order to find out the values of the steroid resources for the future use. the compositions and contents of steroidal sapogenins from 13 domestic plants have been investigated. As a result,Dioscorea nipponica, D. quinqueloba andSmilax china were found to have large amount of diosgenin. And pennogenin inTrillium kamtschaticum andParis verticillata, yuccagenin inAllium fistulosum, hecogenin inAgave americana and neochlorogenin inSolanum nigum were appeared to be major steroidal sapogenins.     

Gender-related symptoms and correlates of alcohol dependence among men and women with a lifetime diagnosis of alcohol use disorders

This study explored gender-related symptoms and correlates of alcohol dependence in a crosssectional study of 150 men and 150 women with a lifetime diagnosis of alcohol use disorders (AUD). Participants were recruited in equal numbers from treatment settings, correctional centres and the general community. Standardized measures were used to determine participants' use of substances, history of psychiatric disorders and psychosocial stress, their sensation seeking and family history of substance use and mental health disorders. Multivariate analyses were used to detect patterns of variables associated with gender and the lifetime severity of AUD. Men had a longer history of severe AUD than women. Women had similar levels of alcohol dependence and medical and psychological sequelae as men, despite 6 fewer years of AUD. More women than men had a history of severe psychosocial stress, severe dependence on other substances and antecedent mental health problems, especially mood and anxiety disorders. There were differences in family history of alcohol-related problems approximating same-gender aggregation. The severity of a lifetime AUD was predicted by its earlier age at onset and the occurrence of other disorders, especially anxiety, among both men and women. The limitations in the generalizability of these findings due to sample idiosyncrasies are discussed.