题名的的撰写规范

题名应简明、具体、确切,能概括论文的特定内容,有助于选定关键词,符合编制题录、索引和检索的有关原则。题名应该避免使用公式和不常见的缩略词、字符、代号等。必要时,可使用本行业通用缩写词。题名一般不宜超过20字。若题名语意未尽,可以用副题名补充说明论文中的特定内容。避免使用陈述句,因为题名主要起标示作用,而陈述句容易使题名具有判断式的语义,且不够精炼和醒目。少数情况（评述性、综述性和驳斥性）下可以用疑问句做题名,因为疑问句有探讨性语气,易引起读者兴趣。同一篇论文的英文题名与中文题名内容上应一致,尽量减少冠词的使用。     

药物的诱变作用和它的DNA的圆二色谱的影响

一个药物若与DNA反应则往往有诱变作用。因此分析药物与DNA的关系是一个重要的课题。已有多种方法,从不同的角度分析药物与DNA之间的相互作用,其中园二色谱(circular dichroism,CD)是一种可靠、灵敏、简便的方法。DNA分子有它特有的CD谱,若药物分子嵌入DNA分子或与之形成复合物,这将改变DNA的构型而导致CD谱的变化。我们试图探索药物的诱变作用和它对DNA的CD谱影响之间的关系。小     

癌的光化学疗法的进展

1924年,有人发现血卟啉在动物及人的恶性肿瘤中聚集,并在光照后发生特异萤光。1960年Lipson研制成血卟啉衍生物(HPD)。1973年起Dougherty和早田义博等进行了大量基础理论研究工作。随着激光医学、光导纤维和纤维内窥镜的发展,已有效地应用于临床。     

肺癌的抗体治疗的研究进展

肺癌的传统疗法效果不够理想，用抗体治疗肺癌是一较为有效的方法。目前主要有5类抗体用于治疗肺癌：（1）西妥昔单抗(Cetuximab)、ABXEGF(Panitumumab)、Matuzumab（EMD72000）和曲妥珠单抗(Herceptin)等，这类抗体通过结合肿瘤细胞表面分子抑制细胞生长，具有较好的疗效，     

多拉的梦：谁的声音——斯垂彻的、弗洛依德的或多拉的?

通过梦发掘潜意识为弗洛依德的重大贡献,他首次从科学的角度对梦进行了系统性的研究。弗洛依德在1900年出版的《梦的解析》(Die Traumdeutung)一书至今仍是许多心理学家教学和临床运用的范本。分析梦是我们考察潜意识的绝佳途径,它已经成为精神分析的基本技术之一。本文不仅详细地描述了如何分     

关于数字的使用的要求

本刊执行GB／T15835-1995《关于出版物上数字用法的规定》。公历世纪、年代、年、月、日、时刻和计数、计量均用阿拉伯数字。书写百分数范围，前一个数字的百分符号不能省略，如：5％～30％，不要写成“5～30％”。     

上帝造的与人造的

我现在越来越喜欢使用类比这种思考方式，也越来越喜欢采用比喻的说法。我频繁使用上帝这个词，并不意味着我相信一个有人格的上帝，一个可以与人沟通的神。我只是采用了“上帝”这个比喻性的、拟人的说法。当然我也可以辩称，我所说的上帝是爱因斯坦或者斯宾诺莎的上帝，就是自然（规律）本身。     

直肠癌的辅助放化疗的临床研究

直肠癌是常见的消化道恶性肿瘤，手术是直肠癌的主要治疗手段，放化疗对可手术直肠癌是重要的辅助治疗手段。无论术前或术后放疗均可提高局部控制，术前放疗可增加保肛的机率，放疗的方式以常规分割较佳。术后放疗在中度复发危险的患者中对生存的影响与化疗相似，但需要两者对局控的资料。本文综述的是术前放疗、术后放疔以及术前与术后放疗的比较。     

原发灶不明的黑色素瘤的治疗

本文报告1045例黑色素瘤中的64例原发灶不明的黑色素瘤的治疗与疗效。全组病例中,男性39例(59％),女性25例(38％),年龄2～73岁,平均44.5岁(中位年龄42.7岁)。34例仅有单部位的侵犯,其中位于腋窝区者10例(29％),位于腹股沟区者8例(23％),位于颈部者11例(32％),位于皮下组织者4例(12％),位于其他部位者1例(3％)。单部位侵犯限于一个淋巴结区者(腋窝、腹股沟、颈部)共计29例。另外30例有2个或2个以上部位的侵犯。     

Mechanism of riboflavin deficiency facilitating carcinogenesis of N-nitrosamine--effect on carcinogen-metabolizing enzymes

Previous studies have demonstrated the facilitating effect of riboflavin deficiency on the carcinogenesis of the liver of rats induced by N-nitrosamine. However, the mechanism was still not clear. In the present investigation, the alterations of microsomal carcinogen-metabolizing enzymes of rat liver during riboflavin-deficiency with simultaneous administration of nitrosodimethylamine (NDMA) were studied. The results showed that the enzyme activities of hepatic microsomal cytochrome P-450 and NDMA demethylase of riboflavin deficient rats and riboflavin deficient rats receiving NDMA were increased and significantly different from the control rats (P less than 0.05). The enzyme activities of hepatic microsomal NADPH-cytochrome P-450 reductase of riboflavin deficient rats and riboflavin deficient rats receiving NDMA were significantly decreased (P less than 0.01). All the alterations disappeared after supplying riboflavin to the deficient rats. This result indicates that the effect of riboflavin deficiency on carcinogen-metabolizing enzymes of rat liver is reversible.     

Effects of riboflavin deficiency on metabolism of nitrosamines by rat liver microsomes

The effects of riboflavin deficiency on the metabolism of N-nitrosodimethylamine [(DMN) CAS: 62-75-9] and other nitrosamines were examined in rats. After weanling rats were put on a riboflavin-deficient diet, the development of the deficiency was monitored by the growth rate and the erythrocyte glutathione reductase activation coefficient. In the riboflavin-deficient rats, the liver microsomal NADPH-cytochrome c reductase activity was lower but the cytochrome P450 content was higher than that of the control. The metabolism of DMN was dependent on the severity of the deficiency. During mild deficiency, which was observed mainly with Sprague-Dawley rats, the microsomal DMN demethylase (DMNd) activity was elevated 30-80%, but the metabolism of N-nitrosomethylbenzylamine (CAS: 937-40-6) and three other nitrosamines was slightly decreased. Dietary restriction in the pair-fed group also caused an elevation of DMNd activity above that of the ad libitum control group due to a partial fasting effect. During severe deficiency, which was observed mainly with Wistar rats, however, the metabolism of DMN, as well as the oxidation of benzo[a]pyrene, was decreased. Preincubation with flavin adenine dinucleotide and flavin mononucleotide enhanced the DMNd activity of the microsomes from riboflavin-deficient rats but not that from control rats. The results suggest that, depending on the alterations of the monooxygenase enzyme system during the development of the deficiency, riboflavin deficiencies may have different effects on the metabolism of DMN and some other carcinogens.     

Effects of riboflavin on the dimethylnitrosamine demethylase system in the rat liver

The effects of riboflavin on the dimethylnitrosamine [(DMN) CAS: 62-75-9; N-nitrosodimethylamine] demethylase system in inbred F344 rat liver were investigated. Dietary riboflavin deficiency markedly stimulated the activity of DMN demethylase I operating at a low substrate concentration (4 mM), but it caused no change in the activity of DMN demethylase II operating at a high substrate concentration (200 mM). This effect could be reversed by short-term supplementation of the vitamin by a series of three ip injections (0.5 mg/dose/day) to the deficient animals. This dosage regimen of riboflavin did not change the activity of DMN demethylase I in the normal animals. The study in vitro demonstrated that flavins were inhibitory to DMN demethylase I. The enzyme activity in the microsomes of both control and deficient animals was inhibited by preincubation with flavins, suggesting that the interaction between flavins and the enzyme rendered the enzyme inactive. Flavin adenine dinucleotide (FAD) appeared to have a more pronounced effect than riboflavin. In agreement with the earlier observation, DMN demethylase II was unaffected by FAD or riboflavin.     

Grapefruit juice intake does not enhance but rather protects against aflatoxin B1-induced liver DNA damage through a reduction in hepatic CYP3A activity

Influence of grapefruit juice intake on aflatoxin B1 (AFB1)-induced liver DNA damage was examined using a Comet assay in F344 rats given 5 mg/kg AFB1 by gavage. Rats allowed free access to grapefruit juice for 5 days prior to AFB1 administration resulted in clearly reduced DNA damage in liver, to 65% of the level in rats that did not receive grapefruit juice. Furthermore, rats treated with grapefruit juice extract (100 mg/kg per os) for 5 days prior to AFB1 treatment also reduced the DNA damage to 74% of the level in rats that did not receive grapefruit juice. No significant differences in the portal blood and liver concentrations of AFB1 were observed between grapefruit juice intake rats and the controls. In an Ames assay with AFB1 using Salmonella typhimurium TA98, lower numbers of revertant colonies were detected with hepatic microsomes prepared from rats administered grapefruit juice, compared with those from control rats. Microsomal testosterone 6beta-hydroxylation was also lower with rats given grapefruit juice than with control rats. Immunoblot analyses showed a significant decrease in hepatic CYP3A content, but not CYP1A and CYP2C content, in microsomes of grapefruit juice-treated rats than in non-treated rats. No significant difference in hepatic glutathione S-transferase (GST) activity and glutathione content was observed in the two groups. GSTA5 protein was not detected in hepatic cytosol of the two groups. In microsomal systems, grapefruit juice extract inhibited AFB1-induced mutagenesis in the presence of a microsomal activation system from livers of humans as well as rats. These results suggest that grapefruit juice intake suppresses AFB1-induced liver DNA damage through inactivation of the metabolic activation potency for AFB1 in rat liver.     

Carcinogenicity studies of tobacco extract in vitamin A-deficient Sprague-Dawley rats

Long-term carcinogenicity studies were carried out in male Sprague-Dawley rats maintained on vitamin A-sufficient (SLO+) and vitamin A-deficient (SLO-) diets and treated with tobacco extract (TE). Three-week-old rats received by gavage a total dose of 860 mg of TE at a daily dose of 3 mg/rat over a period of 21 months. Besides tumorigenicity, drug-metabolizing phase I and phase II enzymes in lung and liver as well as vitamin A and C levels in plasma and liver were measured at 12 and 21 months of age. The cumulative tumor incidence in TE-treated SLO- rats was significantly higher (77-100%) than that observed in TE-treated SLO+ rats (20-22%). Furthermore, SLO+ rats treated with TE showed lung and forestomach tumors, whereas TE-treated SLO- rats showed a preponderance of pituitary adenomas (87%). It was observed that TE treatment increased the activity of the hepatic and pulmonary phase I enzymes and decreased the glutathione/glutathione S-transferase detoxification system at both time points in SLO- rats. On TE treatment the vitamin A levels in the liver and plasma were significantly decreased with a concurrent increase in vitamin C levels. The data show that a vitamin A-deficient diet renders male Sprague-Dawley rats more susceptible to TE treatment than the vitamin A-sufficient diet, an effect which was associated with the augmented induction of P-450 content and activities and depletion of the glutathione/glutathione S-transferase pathway by TE.     

Comparison of aflatoxin B1-DNA binding and glutathione conjugate formation by liver preparations from rats of different ages.

The capability of the newborn rat liver to detoxify aflatoxin B1 (AFB1), a potent hepatocarcinogen is not well understood. Our present results show that immature rats are deficient in the hepatic key factors involved in biotransformation of AFB1. The activities of cytosolic glutathione S-transferases and microsomal cytochrome P-450 along with cellular glutathione (GSH) content show postnatal developmental changes. The ability of hepatic subcellular preparation from newborn rats to convert AFB1 to its reactive epoxide form, is reported for the first time in this communication. Epoxidation of [3H]AFB1 in the presence of liver microsomes from different age-groups as measured by its adduct formation to calf thymus DNA in vitro shows that newborn rats are capable of catalyzing only minimal AFB1-DNA binding compared with that of adults. Addition of cytosolic fraction of various age groups to the system suggests that young rats are less efficient in modulating the binding as compared with adults. The amount of AFB1-GSH conjugate formed is also significantly higher when adult GSH S-transferase is involved in the system. These observations show that immature liver is less efficient than a mature organ in handling a chemical carcinogen and the metabolism of AFB1 by neonatal liver differs from that in the adult.     

Riboflavin deficiency and esophageal cancer: a case control-household study in the Caspian Littoral of Iran

BACKGROUND: In a case-household-control-household study in two very high and low esophageal cancer (EC) risk regions of the Caspian Littoral of Iran, a total of 21 cases (12 subjects from the high risk and 9 subjects from the low-risk region) with a total of 91 household members (57 subjects from the high risk and 34 subjects from the low-risk region) were investigated. Cases were matched for sex and age (+/-5 years) with non-blood relative controls. METHODS: A standard 24-h dietary recall questionnaire was used to estimate riboflavin intake. The erythrocyte glutathione reductase activity coefficient (EGR-AC) was measured to assess riboflavin status. The Student t-test was used to test differences, and chi2 analysis was applied to test associations. Odds ratios (ORs) and corresponding 95% confidence intervals (CIs) were also calculated. RESULTS: Results indicated that in both regions, the mean daily intake of riboflavin for cases was less than that of the controls (0.66+/-0.43 mg/day versus 0.82+/-0.37 mg/day) whereas for their households, it was virtually the same. Both cases and control households showed riboflavin deficiency in two regions, with higher deficiency in the high risk area. Statistical analysis revealed significant differences between the two regions for EGR-AC (P<0.001). Odd ratios indicated that the risk of developing EC for persons living in riboflavin-deficient households was more than twice of non-deficient households. CONCLUSION: Therefore, this study suggests that riboflavin deficiency may play an important role in the etiology of esophageal cancer in the Caspian Littoral of Iran.     

Effect of glutathione depletion on the hepatotoxicity and covalent binding rat liver macromolecules of N-hydroxy-2-acetylaminofluorene

Glutathione plays an important role in the protection of the liver against several hepatotoxins. The hepatocarcinogen N-hydroxy-2-acetylaminofluorene is converted in the rat in vivo to reactive metabolites that bind covalently to cellular macromolecules. These metabolites may also react with glutathione, resulting in the formation of glutathione conjugates and in the detoxification of reactive metabolites. The role of glutathione in detoxification was investigated by depletion of glutathione in the rat in vivo with diethyl maleate. When rats were pretreated with diethyl maleate, 45 min before the administration of N-hydroxy-2-acetylaminofluorene, excretion of 2-acetylaminofluorene:glutathione conjugates in bile was decreased by 60% as compared to controls. However, total covalent binding to rat liver protein was not increased, and total binding to DNA was even decreased (p less than 0.1), apparently at the expense of the acetylated carcinogen-DNA adducts. Formation of deacetylated, 2-aminofluorene adducts to DNA was not affected by diethyl maleate. Pretreatment with diethyl maleate had no major effect on the acute hepatotoxic effects of N-hydroxy-2-acetylaminofluorene. The results indicate that glutathione does not play a vital role in the detoxification of reactive metabolites generated from the carcinogen N-hydroxy-2-acetylaminofluorene, since glutathione is not very effective in competing with macromolecules for trapping of reactive metabolites of N-hydroxy-2-acetylaminofluorene. Thus, 1 mM glutathione did not decrease the covalent binding of 2-acetylaminofluorene-N-sulfate (one of the main reactive metabolites that is formed in vivo) to DNA in vitro, while 10 mM glutathione decreased the covalent binding to RNA by only 20% and to DNA by only 40%.