可能发生急性职业中毒的化学物质（续二）

可能发生急性职业中毒的化学物质（续二）六氟化硒ＰＮ：ＳＥＬＥＮＩＵＭ－ＨＥＸＡＦＬＵＯＲＩＤＥ－ＲＮ：７７８３－７９－１ＩＤＬＨ：＋５ｐｐｍ亚砷酸钠ＰＮ：ＳＯＤＩＵＭ－ＡＲＳＥＮＩＴＥ－ＲＮ：７７８４０－４６－５ＩＤＬＨ：＋Ｃａ蒽ＰＮ：ＡＮＴＨＲＡＣ...     

西门子SOMATOM ART CT灯丝电流减少故障维修

故障现象：１．ＣＴ开机后，软件拷贝检索正常，直到出现ＳＯＭＡＴＯＭＡＲＴＶＤ１０８表格后出现Ｒｅｓｅｔ，经过几次Ｒｅｓｅｔ后，机架面板指示灯才能正常显示；２．在以后的扫描过程中也老出现Ｒｅｓｅｔ，床体锁住不能运动，Ｒｅｓｅｔ后又能继续扫描；３．查询系统报告，故障记录如下：ａ．ＥＩ０２１７ｂ．ＥＩ０１０５ｃ．ＥＸ０８２１ＥＸＰ－ＦＩＬ－ＬＯＷ－ＥＲＲ（％Ｓ）ｄ．ＥＸ０８２４ＰＵＳＨ－ＥＲＲ（％Ｓ）分析检修：１．排除计算机系统及软件原因。关掉机架电源，单启动计算机系统，程序自检能通过，说明计算机系统…     

可能发生急性职业中毒的化学物质（续前）

可能发生急性职业中毒的化学物质（续前）硫酸钴ＰＮ：ＣＯＢＡＬＴＯＵＳ－ＳＵＬＦＡＴＥＲＮ：１０１２４－４３－３ＭＦ：＊Ｃｏ－Ｏ４－ＳＩＤＬＨ：＋２０ｍｇ／ｍ３（以钴计）氰化钙ＰＮ：ＣＡＬＣｌＵＭ－ＣＹＡＮＩＤＥＲＮ：５９２－０１－８ＭＦ：＊Ｃ２－Ｃａ...     

1999年上半年境外医疗器械产品注册情况(一)

序号产品名称生产厂国家注册号１气腹机ＷＩＳＡＰＧＥＳＥＬＬＳＣＨＡＦＴＦＵＲＷＩＳＳＥＮＳＣＨＡＦＴＬＩＣＨＥＮＡＰＰＡＲＡＴＥＢＡＵＭＢＨ德国９９－０００１２心电电极ＭＳＢ（Ｓ－Ｅ－Ａｓｉａ）Ｌｔｄ．新加坡９９－０００２３外科手术电极ＭＳＢ（Ｓ－Ｅ－Ａｓｉａ）Ｌｔｄ．新加坡９９－０００３４ＣＵＢＡＣｌｉｎｉｃａｌ超声骨密度仪ＭｃＣｕｅＰｌｃ英国９９－０００４５超乳玻切系统ＧｅｕｄｅｒＧｍｂＨ德国９９－０００５６听觉诱发电位系统ＩＣＳＭｅｄｉｃａｌＣｏｒｐｏｒａｔｉｏｎ美国９９－０００６７眼震电…     

国外求购信息

国外求购信息１．法国求购消毒剂ＤＩＳＩＮＦＥＣＩ－ＡＮＩ－ＳＦＯＲＭＥＤＩＣＡＬ＆ＣＯＳＭＥＩ－ＩＥＣＳＦＩＥＬＤ，ＤＩＳＩＮＦＥＣＩ’ＡＮＴＳＦＯＲＦＯＯＤＩＮＤＵＳＴＲＹＭＲ．ＧＡＵＴＨＩＥＲ　ＰＬＯＵＶＩＥＲ　ＣＯＭＥＦＩ４０ＲＵＥＥＵＧＥＮＥ...     

3种煤尘细胞毒性与其成纤维细胞效应的关系

采用ＳＥＭ／ＥＤＸＳ和ＸＰＤ检测不同变质期３种煤尘的化学元素和矿物成分．将不同浓度的煤尘作用于大鼠肺泡巨噬细胞（ＡＭ），测定粉尘－ＡＭ上清液中ＰＧＥ２、ＭＤＡ、ＬＤＨ含量和细胞存活率。将煤尘和标准石英作用过的粉尘－ＡＭ上清液，再作用于成纤维细胞。选用３Ｈ－ＴｄＲ同位素掺入法、ＭＴＴ法和放射自显影法，检测２ＢＳ细胞的增殖能力；对二甲氨基苯甲酸法测定２ＢＳ细胞胶原合成；在透射电镜下，观察２ＢＳ细胞超微结构变化．并测算其粗面内质网的扩张程度．结果显示：３种煤尘细胞毒性大小顺序Ａ＞Ｍ＞Ｆ，并不与其致纤维化效应强弱的顺序（Ｆ＞Ａ＞Ｍ）相一致。这可能与其矿物成分有关。     

21-氨基类固醇抗石英细胞毒性及抑制其促成纤维细胞生长的研究

目的 研究２１－氨基类固醇（Ｌazaroid,Ｕ－７５４１２Ｅ）在体外对石英毒性的抑制作用。方法 观察体外培养的肺汔巨噬细胞（ＡＭ）释放Ｈ２Ｏ２、乳酸脱氢酶（ＬＤＨ）、超氧化物歧化酶（ＳＯＤ）和β－Ｎ－乙酰氨基葡萄苷酶（ＮＡＧ）的水平,评价Ｕ７５４１２Ｅ对石英细胞毒性的消除能力;电子自旋共振俘获法评价Ｕ－７５４１２Ｅ清除石英催化Ｈ２Ｏ２产生．ＯＨ的作噻唑蓝比色法比较Ｕ－７５４２１Ｅ对矽肺大鼠肺泡ＡＭ促成纤     

IQ CT阴极输出模块故障维修实例

故障现象机架工作正常,控制台高压ＲＥＡＤＹ灯不能点亮,即高压不能上电。打开机架,在高压控制及输出部分分别发现模拟控制板（ＡＮＡＬＯＧＹＣＯＮＴＲＯＬＬＢＯＡＲＤ）的ＤＳ７灯点亮,提示板上 １５Ｖ控制电源（ １５ＶＳＷＩＴＣＨ）故障;在阴极输出模块（ＣＡＴＨＯＤＯＵＴＰＵＴＭＯＤＵＬＥ）上ＤＳ９灯亮,提示模块 １５Ｖ控制电源（ １５ＶＳＷＩＴＣＨ）故障;在逆变诊断控制板（ＩＮＶＥＲＴＥＲＤＩＡＧＮＯＳＴＩＣＢＯＡＲＤ）上的ＤＳ１５灯点亮,提示板上 １５Ｖ控制电源（ １５ＶＳＷＩＴＣＨ）故障;在系统控制板（ＳＹＳ…     

监护仪的选购、使用及维护

多参数监护仪被广泛地应用于医院急诊室、重症监护室、手术室及各病区病房中 ,它是医院医疗设备中量多面广的一种诊断设备。市场上监护仪种类很多 ,在资金许可的情况下 ,一般医院都会首选品牌机产品。目前国内使用的主要品牌机有ＨＰ(惠普 )、ＳＰＡＣＥＬＬＡＳＳ (太空 )、ＩＮＶＩＶＯ (鹰威 )、ＭＤＥ、Ｓ＆Ｗ、ＯＨＭＥＤＡ (欧美达 )、ＭＩＬＬＥＮＮＩＡ (米兰 )、ＳＩＥＭＥＮＳ (西门子 )、ＭＡＲＱＵＥＴＴＥ (麦克 )、ＤＡＴＥＸ (德恩 )、ＣＲＩＴＴＩＫＯＮ (强生 )等。我院先后选用了西门子监护系统 ,惠普、米兰、鹰威、Ｓ＆…     

卫生防疫计算机网络初探

经过技术调研、方案论证、网络实施和调试运行等阶段工作,深圳市罗湖区卫生防疫站计算机网络系统（ＳＨＥＮＺＨＥＮＬＵＯＨＵＰＵＢＬＩＣＨＥＡＬＴＨＡＮＤＡＮＴＩ－ＥＰＩＤＥＭＩＣＳＩＮＦＯＲＭＡＴＩＯＮＮＥＴＷＯＲＫＳＹＳＴＥＭ,ＳＺＬＨＰＨＮＥＴ）已如...     

The unique correlation between anti-mutagenicity of human saliva and change in body weight

The purpose of this study was to investigate the effect of weight reduction on the anti-mutagenicity of human saliva. Subjects were 16 male college judo players. The anti-mutagenicity of the saliva was measured using the umu test. There was an inhibiting effect of the saliva on the mutagenicity of AF-2. However, a modifying effect of the saliva on Trp-P-1 was not observed. On the day before a competition and 7 days after the competition, the inhibiting capacity of the saliva for the mutagenicity of AF-2 decreased and increased in two non-weight reduction and two weight reduction groups, respectively. However, on the day before the competition, the changed body weights (r=−0.77, p<0.01) and BMI (r=−0.77, p<0.01) were significantly correlated with that of the inhibiting capacity of the saliva for the mutagenicity of AF-2. In addition, the BMI at 20 days before the competition was not significantly but markedly correlated with it (r=0.50, p=0.057). At 7 days after the competition, however, these correlations were not found. These findings suggest a unique correlation between the anti-mutagenicity of human saliva and body weight or BMI.     

Daily lifestyles and anti-mutagenicity of saliva

Objectives The purpose of this study was to investigate the relation between lifestyle and the antimutagenicity of saliva. Methods Subjects were 52 healthy female university students. The collection of the saliva samples and the lifestyle measurements were carried out for them. The anti-mutagenicity of the saliva was measured using the umu test. Results With regard to the lifestyle items, only “nutrient balance” tended to contribute positively to the inhibiting capacity of the saliva on the mutagenicity of AF-2. In addition, there was a significant inverse correlation between the score of 7 other items and the inhibiting capacity of the saliva (r=−0.32; p<0.05). We also found a significant relation between their tea and/or coffee consumption and the inhibiting capacity of the saliva. Conclusions These findings suggest that the inhibiting capacity of saliva worked to decrease mutagen levels that were enhanced by poor lifestyle. In addition, “nutrient balance” may contribute to the inhibiting capacity of the saliva independent of 7 other items. With regard to the tea and/or coffee consumption. further studies should be carried out.     

Transient exposure to coffee as a trigger of a first nonfatal myocardial infarction

BACKGROUND: The effects of coffee on myocardial infarction are uncertain. We hypothesize that coffee in the presence of predisposing factors can induce a cascade of events that, through sympathetic nervous activation, can induce the onset of myocardial infarction. METHODS: We recruited 503 incident cases of nonfatal myocardial infarction between 1994 and 1998 in Costa Rica. We used a case-crossover design to calculate relative risks (RRs) and 95% confidence intervals (95% CIs). RESULTS: The RR of myocardial infarction in the hour after coffee intake was 1.49 (95% CI = 1.17-1.89). Occasional coffee drinkers (< or =1 cup/day, n = 103) had a RR of myocardial infarction of 4.14 (2.03-8.42), moderate coffee drinkers (2-3 cups/day, n = 280) had a RR of 1.60 (1.16-2.21), and heavy coffee drinkers (> or =4 cups/d, n = 120) had a RR of 1.06 (0.69-1.63; P = 0.006, test of homogeneity). Patients with 3 or more risk factors (n = 101) had a RR of myocardial infarction of 2.10 (1.30-3.39), whereas patients with fewer than 3 risk factors (n = 396) had a RR of 1.39 (1.04-1.82; P = 0.15, test of homogeneity); and RR was 1.72 (1.30-2.30) among sedentary patients compared with 1.07 (0.66-1.72) among nonsedentary (P = 0.10, test of homogeneity). CONCLUSIONS: The findings indicate that coffee intake may trigger myocardial infarction. The association is particularly strong among people with light/occasional intake of coffee (< or =1 cup/day), with sedentary lifestyle, or with 3 or more risk factors for coronary heart disease.     

无机砷对肝细胞转录因子Nrf2及其调控蛋白表达影响

目的探讨不同时间和不同浓度亚砷酸钠(NaAsO2)暴露对Chang肝细胞株NF-E2相关因子2(Nrf2)、及其调控的下游抗氧化酶NAD(P)H:醌氧化还原酶1(NQO1)和血红素单加氧酶-1(HO-1)蛋白表达的影响。方法25μmol/L NaAsO2作用Chang肝细胞2、4、6、12和24 h;或不同浓度的NaAsO2(10、25和50μmol/L)作用Chang肝细胞6 h,免疫印迹法(western blot)检测细胞内Nrf2、NQO1和HO-1的蛋白表达情况。结果 25μmol/L的NaAsO2可以明显诱导Chang肝细胞Nrf2、NQO1和HO-1的蛋白表达(P<0.01);Nrf2蛋白2 h开始明显诱导,4 h表达水平最高,此后随暴露时间的延长虽然表达有所下降,但持续至24 h仍明显高于对照组;NQO1的蛋白表达水平也从4 h开始增加并持续至24 h;HO-1的蛋白表达则从6 h开始明显诱导,且随暴露时间的继续延长表达持续上升,具有明显的时间-效应关系;10、25和50μmol/L NaAsO2染毒6 h,Nrf2、NQO1和HO-1的蛋白表达均随染毒剂量的增加而大量诱导,具有明显的剂量-效应关系(P<0.01)。结论 NaAsO2暴露能够诱导Chang肝细胞Nrf2、NQO1和HO-1蛋白表达增强,且具有一定的剂量-效应关系。     

1.8 GHz微波对四种化学诱变剂致DNA的损伤作用

目的观察1.8GHz[比吸收率(SAR)为3W/kg]微波(MW)对4种化学诱变剂[丝裂霉素C(MMC)、博莱霉素(BLM)、4-硝基喹啉氧化物(4NQO)、甲基甲烷磺酸酯(MMS)]诱发的人外周血淋巴细胞DNA损伤的影响.方法采用彗星试验体外实验分别在暴露后0 h和21h检测1.8 GHz微波、4种化学诱变剂及微波联合4种诱变剂所诱发的人淋巴细胞DNA损伤.所用的指标为尾长(TL)和尾相(TM).微波辐射和化学诱变剂暴露时间分别为2h和3 h.结果微波组所诱发的DNA损伤与对照组相比,差异无统计学意义(P＞0.05);微波分别与MMC和4NQO的联合暴露组所诱发的DNA损伤明显高于相应浓度的MMC组和4NQO组,差异有统计学意义(P＜0.01或P＜0.05);但微波对BLM和MMS所诱发DNA损伤的增强效应不明显,差异无统计学意义(P＞0.05).结论1.8GHz(SAR为3 W/kg)微波暴露2h并不诱发人淋巴细胞DNA损伤,但能增强MMC、4NQO的DNA损伤效应.     

Enhancement of mutagenicity of 1-nitropyrene by water as a diluent

The mutagenicity of 1-nitropyrene was strongly enhanced in the Salmonella mutagenicity test with the pre-incubation modification when it was dissolved in dimethyl-sulfoxide and diluted with water. The enhancement of mutagenicity was not found in the plate incorporation method and seemed to be common to chemicals which have low solubilities in water. The indications were that the effectiveness of preincubation modification was due to the increased absorption of test chemicals by the Salmonella cells, and that the absorption depends primarily on the solubility of test chemicals in the assay mixture.     

Associations between black tea and coffee consumption and risk of lung cancer among current and former smokers

Although cigarette smoking is a clear risk factor for lung cancer, the other determinants of lung cancer risk among smokers are less clear. Tea and coffee contain catechins and flavonoids, which have been shown to exhibit anticarcinogenic properties. Conversely, caffeine may elevate cancer risk through a variety of mechanisms. The current study investigated the effects of regular consumption of black tea and coffee on lung cancer risk among 993 current and former smokers with primary incident lung cancer and 986 age-, sex-, and smoking-matched hospital controls with non-neoplastic conditions. Results indicated that lung cancer risk was not different for those with the highest black tea consumption (>or=2 cups/day) compared with nondrinkers of tea [adjusted odds ratio (aOR)=0.90; 95% confidence interval (CI)=0.66-1.24]. However, elevated lung cancer risk was observed for participants who consumed 2-3 cups of regular coffee daily (aOR=1.34; 95% CI=0.99-1.82) or >or=4 cups of regular coffee daily (aOR=1.51, 95% CI=1.11-2.05). In contrast, decaffeinated coffee drinking was associated with decreased lung cancer risk for both participants who consumed or=2 cups/day (aOR=0.64; 95% CI=0.51-0.80). These results suggest that any chemoprotective effects of phytochemicals in coffee and tea may be overshadowed by the elevated risk associated with caffeine in these beverages.     

Antiproliferation effect of commercially brewed coffees on human ovarian cancer cells in vitro

Numerous scientific studies have examined the relationship between coffee consumption and an array of medical conditions, including cancer, and yet the direct effect of commercially brewed coffee on cancer cells has not been evaluated. The purpose of this study was to evaluate the antiproliferation effect of 4 different regular and decaffeinated coffee brews and 3 of coffee's bioactive ingredients-caffeine, chlorogenic acids, and caffeic acid-on 2 human ovarian cancer cell lines alone and in combination with cisplatin (CDDP). Antiproliferation IC(50) for Brand A regular and decaffeinated coffee on A2780 cells was 1:70.79 ± 5.66 and 1:55.68 ± 2.00 dilution (vol/vol) in tissue culture medium (mean ± standard error of the mean; N = 12), respectively, and slightly lower on A2780CP70 cells. Three other brands showed lower antiproliferation activity. Antiproliferation IC(50) concentrations of chlorogenic acids and caffeic acid are many folds lower than caffeine. In combination with CDDP, both Brand A coffee brews, and the 3 bioactive compounds, showed additive antiproliferation effect on both cancer cell lines. Flow cytometry analysis showed that coffee treatment induced apoptosis of A2780 and A2780CP70 cells. To our knowledge, this is the first report showing the antiproliferation activity and the additive effect with CDDP of commercially prepared coffee brews on human cancer cell lines.     

Coffee, caffeine, and the risk of liver cirrhosis

PURPOSE: To evaluate the effect of the consumption of caffeine-containing beverages on the risk of symptomatic liver cirrhosis (LC). METHODS: From 1994 to 1998, all the consecutive cirrhotic inpatients admitted in 19 collaborative hospitals for signs of liver decompensation in whom the diagnosis of liver cirrhosis was made for the first time (274 cases) and one or two gender, age, and place of residence pair matched individuals (458 controls) were recruited. Data on years of education, lifetime cigarette use, lifetime intake of alcohol- and caffeine-containing beverages, usual consumption of 180 food items, and on markers of hepatitis B and C viral infection were collected. RESULTS: A statistically significant trend toward lowered cirrhosis risk with increasing exposure to coffee was observed. The LC odds ratios decreased from 1.0 (reference category: lifetime abstainers from coffee) to 0.47 (95% confidence interval: 0.20, 1.10), 0.23 (0.10, 0.53), 0.21 (0.06, 0.74), and 0.16 (0.05, 0.50) in 1, 2, 3, and 4 or more cups of coffee drinkers, respectively. There was no convincing evidence that coffee consumption modifies the effects of the known risk factors of liver cirrhosis (alcohol intake and viruses infection). CONCLUSIONS: These findings support the hypothesis that coffee, but not other beverages containing caffeine, may inhibit the onset of alcoholic and nonalcoholic liver cirrhosis.