Mineral Content in Baltic Herring and Baltic Herring Products

The contents of Fe, Cu, Zn, Mn, K, Mg, Ca, Na, As and Cd in gutted Baltic herring (Clupea harengus membras), in Baltic herring fillets and in two commercial ready-to-eat products made of these were investigated. The fish was caught in 1996–1998 in the northern Baltic. The commercial products were fried fillets and fish burgers. The effects of industrial processing on the mineral composition were studied by collecting samples at several consecutive stages. In the gutted fish the levels of Mn, Ca and Cd were considerably higher than in the fillet mainly due to the bones. Significant differences were also observed in the contents of Mg, Na, Cu and Zn. In the burger process the bones and skin were removed which caused a decrease in the Zn and Ca levels. Ingredients such as salt, spices and flour as part of the formula increased Na and Mn contents in the ready-to-eat products. In the final products the Na content was about 6 times higher than that of the fresh fish.     

As2O3诱导HL-60,K562及NB4细胞的凋亡

目的 :研究三氧化二砷 (As2 O3)对慢性粒细胞K5 6 2 (CML) ,急性粒细胞白血病细胞株HL - 6 0 (AMLM2 )的作用并与细胞株NB4(APLM3)作比较。方法 :采用形态学和流式细胞术观察不同浓度As2 O3 对HL - 6 0 ,K5 6 2及NB4细胞的作用。结果 :As2 O3不仅能诱导NB4的凋亡 ,提高其浓度至 2 .7μM和 8.1μM ,也能诱导K5 6 2 ,HL - 6 0的凋亡。As2 O3 不能诱导三种细胞分化。结论 :As2 O3 对细胞诱导的凋亡是非选择性的且不能诱导分化。     

三氧化二砷抑制人结肠癌裸鼠肝转移的药效 动力学

 目的　研究三氧化二砷(As2O3 ) 对人结肠癌裸鼠肝转移的抑制作用。方法　BALB/ C2nu/ nu 裸 鼠经脾脏接种人结肠腺癌LS2174 T 细胞建立结肠癌裸鼠肝转移模型,于10 min (早期) 、10 天(中期) 、20 天(晚期) 经尾静脉注射As2O3 ,对照组注射生理盐水。观察各组裸鼠体重变化、肝转移结节的数目、大 小、瘤重以及肝脏肿瘤替代率和荷瘤鼠的生存时间。结果　与对照组相比,早期及中期治疗组裸鼠肝转 移结节的数目、大小、瘤重以及肝脏肿瘤替代率和荷瘤鼠的生存时间差异均有统计学意义( P < 0. 05) ,晚 期治疗组差异无统计学意义( P > 0. 05) 。结论　三氧化二砷对人结肠癌裸鼠肝转移有明显的抑制作用, 早期效果优于中晚期。     

三氧化二砷磁性微球的磁性能

目的:制备包裹三氧化二砷的磁性微球,分别测量磁性微球中三氧化二砷和四氧化三铁的含量,并分析其磁性能。讨论包裹三氧化二砷的磁性微球的磁靶向性效果和临床应用的可能性。 方法:采用化学共沉淀法制备四氧化三铁纳米铁磁粒子,采用w/o/w复乳法将纳米铁磁粒子和三氧化二砷包裹于聚D,L乳酸-羟基乙酸共聚物（PLGA）高分子材料中制备成磁性微球,利用全谱直读等离子体原子发射光谱仪测量磁性微球的载药量,分别测量纳米铁磁粒子和磁性微球的磁滞回线,并检验磁性微球的磁分离效果。 结果:纳米铁磁粒子和磁性微球的矫顽力和剩余磁化强度均接近零,但磁性微球的饱和磁化强度大大低于纳米铁磁粒子的饱和磁化强度。磁性微球的磁分离效果明显。 结论:合成的磁性微球外壳由PLGA高分子材料组成,纳米级四氧化三铁分散于PLGA中,壳内是三氧化二砷水溶液。磁性微球具有超顺磁性和磁靶向性。     

How Do Hepatologists Gain Access to Liver Transplant Units?

Liver transplantation has evolved from an experimental treatment to be considered as the most effective therapy for end-stage liver disease and selected cases of hepatocellular carcinoma. Transplant hepatologists must have specific knowledge and abilities to treat those patients who receive a liver transplant. In Spain, approximately 1100 liver transplants are performed each year, and most centers assume both postoperative care and long-term follow-up, which has led to a significant work load in liver transplant units. Despite previous attempts to establish an official training program in hepatology, the Spanish health system does not presently have a specific liver transplant training program to guarantee that future needs of physicians are covered. Collaboration between health authorities and scientific societies is required to guarantee adequate assistance to liver transplant recipients in the future.     

三氧化二砷对骨肉瘤细胞株MG63/dox多药耐药的逆转作用及其机制

目的 探讨三氧化二砷（As2O3）对骨肉瘤阿霉素（ADM）耐药细胞株MG63/dox的逆转作用及其机制。方法 采用不同浓度ADM（1～1000 ng／ml）和As2O3（0.25～16 μmol／L）分别单独作用于MG63和MG63/dox细胞48 h,并选取2 μmol／L As2O3联合不同浓度ADM（1～1000 ng／ml）作用于MG63/dox细胞24、48、72 h,同时设不加任何药物处理的对照组。应用CCK-8法检测两种药物对MG63和MG63／dox细胞增殖的影响,流式细胞术检测2 μmol／L As2O3、200 ng／ml ADM单独或联合处理48 h后MG63／dox细胞的周期分布和凋亡率,蛋白免疫印迹法检测2 μmol／L As2O3、200 ng／ml ADM单独或联合处理48 h后MG63／dox细胞中P-gp、Bcl-2和Bax蛋白的表达水平。结果 As2O3和ADM单药作用于MG63/dox细胞48 h,细胞增殖均未受到影响;4、8、16 μmol/L As2O3和100、200、400、500、1000 ng/ml ADM分别作用于MG63细胞48 h,细胞增殖明显受到抑制（P＜0.05）。As2O3联合ADM抑制MG63／dox细胞增殖的作用明显高于ADM单药组和对照组（P＜0.05）,且抑制作用呈时间依赖性。与对照组相比,两药联合处理组的细胞凋亡率升高,G0／G1期细胞比例降低,G2／M期细胞比例升高,以上差异均有统计学意义（P＜0.05）。两药联合处理组MG63／dox细胞中Bax蛋白表达水平明显升高,而P-gp和Bcl-2蛋白表达水平明显降低,与对照组比较,差异均有统计学意义（P＜0.05）。结论 As2O3联合ADM能够抑制骨肉瘤耐药细胞MG63／dox的增殖,这一作用可能与诱导细胞凋亡、上调Bax表达以及下调P-gp和Bcl-2表达有关。     

As2O3与NaAsO2抑制HeLa细胞生长的研究

目的探讨As2O3和NaAsO2两种砷剂对HeLa细胞的抑制作用.方法培养HeLa细胞,使细胞悬液浓度为105个/mL,用四甲基偶氮唑蓝还原反应(MTT法),倒置显微镜观察两种砷剂对HeLa细胞的作用后细胞形态的变化.结果两种砷剂As2O3和NaAsO2对HeLa细胞均有抑制作用,随着药物浓度的增加,HeLa细胞存活率逐渐下降并存在剂量反应关系,显微镜下观察,三角形的活细胞逐渐减少而圆形的死亡细胞逐渐增加,As2O3的作用比NaAsO2作用强,对照组均未见上述变化. 结论两种砷剂对HeLa细胞均有抑制作用,As2O3的作用比NaAsO2作用强.     

三氧化二砷对人肺腺癌细胞的细胞毒作用及其机制

背景与目的:三氧化二砷(arsenictrioxide,As2O3)应用于急性早幼粒细胞性白血病(acutepromyelocyticleukemia,APL)的临床化疗已显示较好疗效。目前,已开展了将As2O3用于治疗胃癌、头颈部癌和食管癌等实体瘤的实验研究。本研究旨在探讨As2O3对人肺腺癌SPCA1细胞的毒性及其作用机制。方法:MTT法检测As2O3对SPCA1细胞的生长抑制作用;流式细胞术测定经不同浓度As2O3处理后的SPCA1细胞的细胞周期改变、凋亡相关蛋白Fas和Bcl-2阳性细胞百分率及细胞内钙离子(IECa2+)含量变化。结果:As2O3可显著抑制SPCA1细胞生长增殖,且呈剂量-效应关系(r=0.973,P<0.05),其IC50为8.56μmol/L;As2O3能显著增加Fas蛋白表达和IECa2+含量(P<0.05),并使细胞周期阻滞在G2/M期,但对Bcl-2表达无影响(P>0.05)。结论:As2O3对SPCA1细胞有显著的毒性作用,其机制可能与上调Fas表达和增加IECa2+含量及阻滞细胞周期有关。     

As2O3和全反式维甲酸对人宫颈癌HeLa细胞生长的影响

目的 探讨As2O3和全反式维甲酸(ATRA)对人宫颈癌HeLa细胞体外生长的影响及其机制.方法 采用不同浓度As2O3和ATRA分别作用于人官颈癌HeLa细胞,观察细胞形态;采用四甲基偶氮唑蓝(MTT)比色法检测细胞生长情况;半定量逆转录聚合酶链反应(RT-PCR)和Westernblot法检测细胞中N-myc下游调节基因1(NDRG1)mRNA和蛋白的表达.结果 As2O3和ATRA能够抑制宫颈癌HeLa细胞生长,12.5 μmol/L As2O3处理HeLa细胞48 h的抑制率为(36.5±1.2)%,明显高于同时间低浓度组;1 × 10-5mol/LATRA处理HeLa细胞48 h的抑制率为(23.5±3.1)%,明显高于同时间低浓度组,并且同浓度的药物处理72 h的抑制率高于处理48 h的抑制率,呈浓度和时间依赖性(P<0.05).As2O3和ATRA能够从分子水平和蛋白水平上调宫颈癌HeLa细胞中NDRG1基因的表达,12.5 μmol/L As2O3和5×10-6mol/L ATRA处理HeLa细胞后,NDRG1 mRNA表达量分别为0.942±0.169和0.894±0.138,明显高于低浓度组的表达量;12.5 μmol/LAs2O3和5×10-6 mol/LATRA处理HeLa细胞后,NDRG1蛋白表达量分别为1.220±0.202和1.233±0.103,明显高于低浓度组的蛋白表达量.结论 As2O3能够抑制宫颈癌HeLa细胞生长,其抑制作用与NDRG1基因的表达上调相关.

Abstract：

Objective To study the effect of arsenic trioxide (As2O3 ) and all-trans retinoic acid ( ATRA ) on human cervical carcinoma HeLa cell line.Methods HeLa cells were treated with As2O3 and ATRA.The cell proliferation was evaluated by MTT assay.The expressions of NDRG-1 protein and mRNA were determined by Western blot and RT-PCR analysis.Results MTT assay showed that As2O3 and ATRA inhibited the growth of human cervical carcinoma HeLa cells in vitro in a dose- and time-dependent manner.Western blot and RT-PCR techniques showed that As2O3 and ATRA down-regulated the expressions of NDRG-1 protein and mRNA (P < 0.05 ) .Conclusion As2O3 and ATRA can significantly inhibit the growth and proliferation of HeLa cells.The reason of these changes may be related with the down-regulation of expression of NDRG-1.     

Changes in serum thioredoxin among individuals chronically exposed to arsenic in drinking water

It is well known that oxidative damage plays a key role in the development of chronic arsenicosis. There is a complex set of mechanisms of redox cycling in vivo to protect cells from the damage. In this study, we examined the differences in the levels of serum thioredoxin1 (TRX1) among individuals exposed to different levels of arsenic in drinking water and detected early biomarkers of arsenic poisoning before the appearance of skin lesions. A total of 157 subjects from endemic regions of China were selected and divided into arsenicosis group with skin lesions (total intake of arsenic: 8.68-45.71 mg-year) and non-arsenicosis group without skin lesions, which further divided into low (0.00-1.06 mg-year), medium (1.37-3.55 mg-year), and high (4.26-48.13 mg-year) arsenic exposure groups. Concentrations of serum TRX1 were analyzed by an ELISA method. Levels of water arsenic and urinary speciated arsenics, including inorganic arsenic (iAs), monomethylated arsenic (MMA), and dimethylated arsenic (DMA), were determined by hydride generation atomic absorption spectrometry. Our results showed that the levels of serum TRX1 in arsenicosis patients were significantly higher than that of the subjects who were chronically exposed to arsenic, but without skin lesions. A positive correlation was seen between the levels of serum TRX1 and the total water arsenic intake or the levels of urinary arsenic species. The results of this study indicate that arsenic exposure could significantly change the levels of human serum TRX1, which can be detected before arsenic-specific dermatological symptoms occur. This study provides further evidence on revealing the mechanism of arsenic toxicity.