朝鲜淫羊藿酸性多糖的理化特性及对HepG2细胞脂质堆积的改善作用＊

目的 对比研究朝鲜淫羊藿酸性多糖酯化还原前后的理化特性，并探讨其改善油酸诱导的肝癌HepG2细胞脂质堆积活性的差异。方法 采用高效凝胶渗透色谱法测定朝鲜淫羊藿酸性多糖（EFPA）的均一性和分子量，高效液相色谱法测定EFPA和酯化还原后朝鲜淫羊藿酸性多糖（EFPA-R）的单糖组成；采用油酸（OA）处理HepG2细胞诱导建立脂质蓄积模型，不同浓度EFPA与EFPA-R（10、30、100、300 μg·mL^-1）分别和OA共同作用于细胞24 h，采用CCK-8试剂盒测定细胞存活率，油红O染色观察细胞内脂滴蓄积情况，并采用试剂盒测定细胞内总胆固醇（TC）、甘油三酯（TG）含量。结果 EFPA为成分均一的多糖组分，分子量为125.8 kDa，由甘露糖、葡萄糖、半乳糖、葡萄糖醛酸和阿拉伯糖组成，摩尔比为1.7∶7.4∶1.4∶1.8∶1.0，葡萄糖占比最大，EFPA-R由甘露糖、葡萄糖、半乳糖和阿拉伯糖组成，摩尔比为0.8∶10.6∶2.1∶1.0；在10-300 μg·mL^-1范围内，EFPA和EFPA-R对HepG2细胞的抑制作用较弱，作为给药浓度；与空白组相比，模型组细胞中TC、TG含量显著升高（P < 0.01），细胞内红色脂滴显著增多，与模型组相比，EFPA可显著降低细胞中TC、TG含量（P < 0.01），明显减少细胞内红色脂滴（P < 0.05或P < 0.01），EFPA-R干预后细胞则无明显变化。结论 EFPA可明显改善HepG2细胞脂质堆积情况，且呈现剂量依赖性，而半乳糖醛酸（GalA）的存在可能是其抑制HepG2细胞脂质蓄积的关键因素。     

As2O3处理前后K562细胞基因表达变化的基因芯片检测

目的应用基因芯片研究三氧化二砷(As2O3)处理前后K562细胞基因表达的变化.方法提取As2O3处理前后K562细胞的总RNA,纯化为mRNA后再反转录为cDNA.cDNA经限制性内切酶Sau3AI切割后,cDNA片段分别用Cy3和Cy5标记,与自制的包含348个基因片段的胎盘库芯片杂交.结果杂交结果经扫描和软件分析,发现了11个差异表达的基因片段,其中有3个基因片段与细胞凋亡密切相关.结论我们构建的胎盘库基因芯片可以成功地用于研究药物作用前后基因表达的变化.     

谷胱甘肽、自由基在砷剂诱导卵巢癌细胞凋亡中的作用

目的　观察谷胱甘肽、自由基在砷剂诱导卵巢癌细胞凋亡中的作用。方法　砷剂孵育卵巢癌细胞 4 8h后 ,琼脂糖凝胶电泳及流式细胞仪检测细胞凋亡 ,分光光度法检测细胞内谷胱甘肽、活性氧及丙二醛含量。结果　砷剂具有诱导卵巢癌细胞凋亡作用 ,砷剂诱导后细胞内谷胱甘肽含量减少 (P <0 .0 1)、活性氧及丙二醛含量增加(P <0 .0 5 )。结论　氧化还原系统的改变是砷剂诱导卵巢癌细胞凋亡的重要途径之一。     

As_2O_3诱导人肝癌细胞凋亡及对Fas表达和钙含量的影响

化疗在原发性肝癌的综合治疗中占重要地位.为寻找肝癌治疗新的有效药物,我们观察了As2O3对人肝癌细胞株BEL7402的生物学效应,以期为As2O3临床治疗肝癌提供实验依据.     

Arsenical necrosis of the jaws

After a brief historical review of the use of arsenic in dental practice two cases of arsenical necrosis of the jaws, affecting the maxilla and mandible respectively, are reported. Both patients were treated conservatively over an extended period with excellent results. It is concluded that there is no justification, whatsoever, for the use of arsenic in modern dental practice and that, although prolonged, conservative treatment of chemical necrosis of the jaws is preferable to more radical treatment.     

Antipsychotics with inverse agonist activity at the dopamine D3 receptor

Summary In NG 108-15 cells expressing the recombinant human D₃ receptor, dopamine agonists enhance [³H]thymidine incorporation and decrease cAMP accumulation. In these cells, but not in wild type cells, haloperidol, fluphenazine, and various other antipsychotics inhibited basal [³H]thymidine incorporation in a concentration-dependent manner. In contrast, other dopamine antagonists such as nafadotride or (+)AJ 76, two D₃-preferring antagonists, were without effect. The concentration-response curve of haloperidol was shifted to the right in presence of nafadotride, with a potency compatible with its nanomolar apparent affinity as neutral antagonist. Pertussis toxin treatment abolished or markedly reduced the responses to haloperidol or fluphenazine. In contrast, no significant enhancement of cAMP accumulation could be observed, under the influence of haloperidol or eticlopride. These data indicate that some dopamine antagonists behave as inverse agonists, and thus appear to inhibit an agonist-independent activity of the D₃ receptor on [³H]thymidine incorporation pathway, but not on the cAMP pathway.     

Accumulation of carbon disulphide metabolites

Summary Biological monitoring for carbon disulphide (CS₂) exposure performed using the iodine-azide test (IAT) and 2-thiothiazolidine-4-carboxylic acid (TTCA) test in urinalysis of workers with high exposure to CS₂ (112–142 mg/m³, n = 34), workers with low exposure (4–7 mg/m³, n = 16), and non-exposed university workers (n =10). Pre-shift and post-shift urine specimens were collected on three consecutive days in the exposed and for only one day in the non-exposed. According to the findings the specificity and the sensitivity seem to be low for the IAT and high for the TTCA test. Contrary to a previous report all pre-shift urine samples showed negative IATs. The TTCA test was positive in pre-shift urine even after 32 to 63.5 h without exposure, and values tended to increase during consecutive days of exposure in highly exposed workers.The possible health implications of these findings should be further investigated.     

Clinical experience with minimal flow xenon anesthesia

Xenon is a more potent anesthetic than nitrous oxide, and gives more profound analgesia. This investigation was performed to assess the potential of xenon for becoming an anesthetic inspite of its high manufacturing cost. Seven ASA I—-II patients undergoing cholecystectomy (n = 4), hernia repair (n = 2), or mammoplasty (n=l) were studied. Denitrogenation by 15–20 min of oxygen breathing under propofol anesthesia was followed by fentanyl–supplemented xenon anesthesia administered via an automatic minimal flow system which held the oxygen concentration at 30%. Xenon anesthesia lasted 76–228 min and 8–14 1 of xenon (ATPD) was used, of which 5.6–8.1 1 was expended during the first 15 min. Anesthesia appeared to be satisfactory, and the patients woke up rapidly after xenon was discontinued. The automatic system made minimal flow xenon anesthesia easy to administer, but nitrogen accumulation is still a problem. Assuming a xenon price of 10 US $ per litre, the average cost for xenon was about 65 US $ for the first 15 min and then about 25 USS for each subsequent hour of anesthesia.     

Assessment of exposure to arsenic among smelter workers: A five-year follow-up

In a group of 43 smelter workers exposed to inorganic arsenic dust for 13-45 years, nerve conduction velocities (NCVs) were significantly lower in two peripheral nerves as compared with matching referents. With multivariate data analysis, a significant negative correlation was found between cumulative absorption of arsenic and NCV in four examined nerves and the sural amplitude. Clinical symptoms of neuropathy and other symptoms related to arsenic exposure were moderate, though the difference between the groups was significant. The mean total absorption of arsenic was calculated to be less than 5 g, and the maximal absorption about 20 g. These data indicate that the adverse effect of arsenic on the peripheral nerves is dependent on long-term exposure rather than on short-term fluctuations in exposure levels. © 1994 Wiley-Liss, Inc.