光气染毒造成小鼠肺脏的氧化损伤

目的　研究小鼠光气染毒后不同时间对肺脏的氧化损伤作用。方法　 4 0只雄性小鼠 ,随机分为 4组。正常对照组小鼠以空气为对照 ,染毒组小鼠给予 11.9mg/L剂量的光气 ,时间为5min ,分别染毒后 2h、4h、8h ,测定各组小鼠肺脏的湿干比和肺匀浆液的丙二醛 (MDA)含量、总超氧化物歧化酶 (T SOD)活力、还原型谷胱甘肽 (GSH)含量。结果　随着光气染毒时间的增加 ,小鼠肺脏的湿干比显著增加 (P <0 .0 5 ) ;染毒后 4h ,肺组织MDA含量和T SOD活力显著升高(P <0 .0 5 ) ,GSH含量在染毒后 2h显著降低 (P <0 .0 5 )。结论　光气染毒可引起小鼠肺水肿和肺脏氧化损伤。     

光气染毒对小鼠肺Ⅱ型细胞凋亡及血管内皮生长因子的影响

目的　观察光气致肺水肿小鼠肺Ⅱ型细胞发生凋亡情况和血清、肺脏的血管内皮生长因子 (VEGF)、VEGF受体 (Flt1)的变化及肺脏VEGFmRNA的表达。方法　 2 6只二级BALB C小鼠 ,雄性 ,随机分为 2组 :对照组和染毒组 (各 13只 )。对照组小鼠以空气为对照 ,染毒组小鼠给予 11.9mg L剂量的光气 ,时间均为 5min ,染毒后 4h ,分离小鼠原代肺Ⅱ型细胞 ,电镜观察两组小鼠肺Ⅱ型细胞凋亡情况 ,酶联免疫法测定血清和肺脏的VEGF、Flt1的含量及反转录PCR法测定肺脏VEGFmRNA的表达。结果　电镜显示光气染毒肺水肿小鼠原代肺Ⅱ型细胞出现凋亡小体 ;染毒小鼠血清VEGF和肺脏的VEGF、Flt1含量 [(134.0 7± 12 0 .2 6 )、(4 77.76± 98.0 6 )、(12 818.4 8± 2 30 4 .15 )pg ml]明显低于对照组 [(4 4 5 .5 7± 173.30 )、(10 2 6 .87± 4 74 .5 6 )、(2 1976 .5 1± 74 2 1.0 1)pg ml],差异有显著性 (P <0 .0 5 ) ;染毒小鼠血清Flt1含量 [(2 36 9.5 6± 381.70 )pg ml]明显高于对照组 [(1898.0 0± 4 5 3.6 9)pg ml],差异有显著性 (P <0 .0 5 ) ;染毒小鼠肺脏VEGFmRNA表达降低。结论　光气经呼吸道染毒可引起肺水肿小鼠原代肺Ⅱ型细胞发生凋亡 ,使血清VEGF和肺脏VEGF、Flt1降低及肺脏VEGFmRNA表达降低。     

光气致小鼠肺脏细胞DNA损伤和凋亡

目的研究光气致BALB/c小鼠肺水肿模型的肺脏的DNA损伤和凋亡。方法26只二级BALB/C小鼠,雄性,随机分为正常对照组和染毒组,各13只。正常对照组小鼠给予空气,染毒组小鼠给予11·9mg/L剂量的光气,时间均为5min,染毒后4h,比较2组小鼠肺脏的湿干比、病理学变化,单细胞凝胶电泳测定2组肺Ⅱ型细胞DNA损伤情况及对小鼠肺脏进行DNA琼脂糖凝胶电泳。结果11·9mg/L的光气染毒5min,小鼠肺脏湿干比(6·42±1·00)比正常对照组(4·25±0·47)显著增加(P<0·05);光镜下观察肺组织可见肺水肿发生;单细胞凝胶电泳法测定染毒组肺Ⅱ型细胞的尾长、尾部DNA、尾距均显著高于正常对照组(P<0·001);DNA琼脂糖凝胶电泳出现DNA梯状样改变。结论光气染毒可造成小鼠肺水肿,引起肺Ⅱ型细胞发生DNA损伤和肺脏细胞凋亡。     

急性光气吸入对大鼠抗氧化酶及一氧化氮和一氧化氮合酶的影响

目的　研究光气急性吸入对机体抗氧化酶活力以及一氧化氮 (NO)、一氧化氮合酶(NOS)的影响。方法　利用三光气在N ,N 二甲基甲酰胺作用下分解生成光气的方法 ,设对照组采用SD大鼠进行动态恒量染毒 ,2h后处死实验动物 ,取肺组织测定湿干比 ,取全血、血清和肝组织分别测定谷胱甘肽硫转移酶 (GST)、过氧化氢酶 (CAT)、超氧化物歧化酶 (SOD)、谷胱甘肽过氧化物酶 (GSH Px)、NO、NOS活力和总蛋白含量。结果　染毒组实验动物的肺湿干比明显大于对照组 ,差异有显著性(P <0 .0 1) ,血清和肝组织匀浆的GST活力明显升高 ,差异有显著性 (P <0 .0 5 ) ,血清和肝组织中SOD、全血CAT以及全血、血清、肝组织GSH Px活力明显提高 ,差异有显著性 (P <0 .0 5 ) ,血清和肝组织匀浆NO含量明显降低 ,差异有显著性 (P <0 .0 1) ,NOS活力明显升高 ,差异有显著性 (P <0 .0 1)。结论　大鼠光气急性吸入可以明显改变机体抗氧化酶系的活力 ,并且存在着一定程度的急性肝损伤 ,而这种损伤与活性氧密切相关 ,但多种抗氧化酶活力的升高却提示抗氧化治疗非光气急性中毒救治的首选。     

褪黑素对大鼠光气吸入致肺损伤的保护作用

目的 探讨褪黑素(MT)对光气致大鼠肺损伤的抗氧化保护作用及其可能机制.方法 50只SD雄性大鼠随机分为光气染毒组、空气对照组、MT处理组、地塞米松处理组(DX处理组)和阴性对照组,每组10只,除空气对照组外吸入8.33 mg/L光气,染毒5 min,于染毒后1h分别从尾静脉注入MT(10 mg/kg)、地塞米松(2.5 mg/kg)、1％乙醇生理盐水(1 ml/kg),于6h后处死动物,测定肺组织湿干比,支气管肺泡灌洗液中总蛋白含量及中性粒细胞计数以及肺匀浆中丙二醛(MDA)含量,超氧化物歧化酶(SOD)及髓过氧化物酶(MPO)活力;光学显微镜下观察肺组织病理;蛋白质印迹(Western blot)法测定肺组织中诱导型一氧化氮合酶(iNOS)和核转录因子(NF-kB)的蛋白含量.结果 与空对照气组比较,光气染毒组肺湿干比、BALF中中性粒细胞计数及蛋白含量均升高,差异有统计学意义(P＜0.01).光气染毒组大鼠肺组织中的MDA含量、MPO活力较空气对照组明显升高,差异有统计学意义(P＜0.05).与光气染毒组比较,MT处理组MDA含量和MPO活力均降低,SOD活力升高,差异有统计学意义(P＜0.01).与光气染毒组比较,MT处理组和DX处理组iNOS及NF-kB蛋白质表达均降低,差异有统计学意义(P＜0.01).结论 MT对光气致肺损伤有保护作用,其机制可能与清除自由基抗氧化及抑制iNOS、NF-kB的表达有关.     

碳酸缓冲液对大鼠光气肺损伤影响的研究

目的　探讨光气肺水肿形成机理及碳酸缓冲液对大鼠光气中毒的影响。方法　 4 0只SD大鼠被随机分为阴性对照组、阳性对照组、0 2ml碳酸缓冲液治疗组、0 5ml碳酸缓冲液治疗组。光气染毒后 5min ,阳性对照组注射 0 5ml生理盐水 ,两个治疗组分别注射碳酸盐缓冲液 (碳酸缓冲液 :Na2 CO3 /NaHCO3 pH :7 6 ,0 1mmol/L) 0 2和0 5ml,3h后处死采血并开胸取肺 ,用荧光分光法检测脂质过氧化产物丙二醛 (MDA)、还原型谷胱甘肽 (GSH)和氧化型谷胱甘肽 (GSSG) ,测量并计算肺湿干比。结果　与阴性对照组相比 ,光气染毒大鼠血清MDA含量显著升高 (P <0 0 1) ,血清GSH显著降低 (P <0 0 1) ,肝脏GSSG显著升高 (P <0 0 5 ) ,肺湿干比增大 (P <0 0 5 )。与阳性对照组相比 ,给予碳酸缓冲液治疗组血清MDA均显著降低 ,0 5ml碳酸缓冲液对血清MDA的抑制作用更强 (P <0 0 5 ) ;两个碳酸缓冲液治疗组血清GSH升高显著 (P <0 0 5 ) ;治疗组的肺湿干比有所降低 ,但无显著性差异 (P <0 0 5 )。结论　光气中毒后出现氧化损伤 ,抗氧化剂GSH损耗严重 ;给予碳酸缓冲液可以缓解光气中毒肺损伤。     

糖皮质激素治疗二氧化氮致大鼠急性肺水肿实验初步研究

目的 探讨糖皮质激素对二氧化碳(NO2)所致大鼠急性肺水肿的治疗效果.方法 将SD大鼠随机分为空白对照组、染毒组及大、中、小剂量糖皮质激素治疗组,每组6只.空白对照组予净空气平衡30 min,染毒组及大、中、小剂量糖皮质激素治疗组在NO2染毒后分别给予生理盐水2.5 mg/kg和地塞米松6.0、3.0、1.0 mg/kg.测定大鼠肺湿干重比(W/D),用ELISA法测定血浆心房利尿钠肽(ANP)含量、全血超氧化物歧化酶(SOD)活力及血浆中白细胞介素-6(IL-6)、IL-10、肿瘤坏死因子-α(TNF-α)、γ-干扰素(IFN-γ)的含量.结果 与空白对照组比较,大、中、小剂量激素治疗组及染毒组大鼠肺W/D明显升高,差异有统计学意义(P<0.05);与染毒组比较,大、中、小剂量激素治疗组大鼠肺W/D明显降低,差异有统计学意义(P<0.05).与空白对照组比较,大、中、小剂量激素治疗组及染毒组大鼠全血中SOD活力明显降低,差异有统计学意义(P<0.05);与染毒组比较,大、中、小剂量激素治疗组全血中SOD活力无明显改变,差异无统计学意义(P>0.05).与空白对照组比较,染毒组大鼠血浆中ANP含量明显升高,差异有统计学意义(P<0.05);与染毒组比较,大、中、小剂量激素治疗组大鼠血浆中ANP含量明显降低,差异有统计学意义(P<0.05).与染毒组[(68.55±27.84)pg/ml]比较,大、中、小剂量激素治疗组大鼠血浆中TNFα含量[分别为(27.04±8.19)、(40.10±9.09)、(39.76±9.60)pg/ml]明显降低,差异有统计学意义(P<0.05).与染毒组[(29.29±9.31)pg/ml]比较,大、中剂量激素治疗组大鼠血浆中IL-6含量[分别为(15.97±6.18)、(19.69±5.52)pg/ml]降低,差异有统计学意义(P<0.05).与染毒组[(44.38±9.19)pg/ml]比较,大、中、小剂量激素治疗组大鼠血浆中IL-10含量[(23.24±5.14)、(27.78±8.17)、(33.29±10.42)pg/ml]降低,差异有统计学意义(P<0.05).与染毒组[(30.83±6.82)pg/ml]比较,大、中剂量激素治疗组大鼠血浆中IFN-γ含量[分别为(7.21±4.55)、(19.23±4.35)pg/ml]降低,差异有统计学意义(P<0.05).结论 大、中、小剂量糖皮质激素均具有改善肺泡壁和毛细血管的通透性及非特异性的抗炎作用,对肺水肿有明显的治疗作用,在降低炎性因子方面,以大、中剂量激素治疗组效果更为明显.     

光气急性中毒的剂量-反应关系与肺水肿动物模型的建立

目的明确光气急性中毒的剂量-反应关系与其半数致死浓度（LC50）,建立光气中毒肺水肿动物模型,为进一步研究光气损伤机制及防治手段奠定基础.方法小鼠按体重随机分为6组,每组10只,雌雄各半,分别按3.7、4.3、4.7、5.2、5.7、6.3ml给予40%三光气（BTC）;大鼠按2.00、3.03、4.58、6.93、10.50 ml分别给予BTC,动态染毒3 min.随即连续7 d观察其进食、活动及死亡情况.应用改良寇氏法计算小鼠、大鼠光气染毒的LC50.小鼠染毒后4 h,肺脏右叶称量湿重,放入75℃烤箱烘烤24 h,称量肺脏干重,计算肺脏湿干比;取肺脏左叶进行常规HE染色,光镜下观察病理学变化.结果小鼠光气中毒的LC50及其95%可信区间为11.97 g/m^3（9.52～14.42 g/m^3）.大鼠光气中毒的LC50及其95%可信区间为13.81 g/m^3（9.16～14.07 g/m^3）.光气染毒后,小鼠肺湿干比随时间延长呈逐渐上升趋势,2 h时显著高于对照组（P＜0.05）.结论本实验确定了小鼠、大鼠光气染毒3 min的LC50,并依此成功建立了光气中毒肺水肿模型.     

光气染毒小鼠急性肺损伤的浓时积与效应关系研究

目的通过比较光气染毒浓时积（Ct）的两个参数（浓度C与时间t）对染毒小鼠急性肺损伤程度的影响，探讨光气导致急性肺损伤的机制。方法以不同浓时积和固定浓时积不同浓度与时间进行光气染毒，测定肺脏湿干比、丙二醛（MDA）含量和髓过氧化物酶活力以及血清中MDA含量。结果随染毒浓时积增加，小鼠中毒死亡率增加（P〈0．001）；浓时积固定为12ml·min时，染毒浓度增加，小鼠中毒死亡率增加（P〈0．01），肺湿干比增加（P〈0．001），肺脏髓过氧化物酶活力和MDA浓度升高（P〈0．05）。结论光气染毒随浓时积增加，动物中毒死亡率升高，但在浓时积相同的条件下，暴露毒剂的浓度与暴露时间对急性中毒的影响不同；暴露毒剂的浓度高低对中毒程度的影响远大于暴露时间的影响，短时间高浓度的光气吸入会比低浓度长时间的光气吸入造成更为严重的肺部损伤。     

孕期二苯基甲烷二异氰酸酯暴露对仔鼠睾丸抗氧化能力的影响

目的 研究孕期二苯基甲烷二异氰酸酯(MDI)暴露对子代雄性小鼠性成熟后睾丸组织中超氧化物歧化酶(SOD)、一氧化氮合酶(NOS)活力及丙二醛(MDA)、一氧化氮(NO)含量的影响.方法 妊娠小鼠随机分成玉米油对照组和3个染毒剂量组,染毒剂量分别为68.75、137.50、275.00 mg/kg.每组织于妊娠第14天开始每日灌胃染毒,持续至母鼠自然分娩.待性成熟后用分光光度法检测雄性仔鼠睾丸组织匀浆中SOD、NOS活力及MDA、NO含量.结果 137.50 mg/kg组SOD活力为297.10±49.98,275.00mg/kg组SOD活力为345.96±44.76,与对照组(450.39±92.82)比较,差异均有统计学意义(P<0.01或P<0.05);3个染毒剂量组总NOS活力分别为2.06±0.77、1.91±0.45、2.19±0.33,与对照组(3.28±0.72)比较,差异有统计学意义(P<0.01);染毒组NO和MDA含量均低于对照组,但差异无统计学意义(P>0.05).结论 孕期MDI暴露可明显抑制SOD和总NOS活力,对雄性仔鼠性成熟后睾丸组织中NO和MDA含量无影响.     

Calcium intake in the elderly: validation of a dietary questionnaire

Epidemiological studies of calcium and osteoporosis have been hampered by the lack of a suitable tool for assessing calcium intake. This report describes a new frequency and amount questionnaire for measuring present and past calcium intake in the elderly. The validity of the questionnaire was tested against two commonly used standards of dietary assessment, five-day duplicate diets and seven-day weighed dietary inventories. The resulting correlation coefficients were, respectively, r = 0.76 and r = 0.69, while that for repeatability was r = 0.84. Furthermore, the questionnaire categorized subjects into thirds of the distribution of intake with almost no gross misclassification. It is suggested that the present findings may be extended to the majority of normal, healthy elderly subjects, implying wide application for the questionnaire in the assessment of calcium intake in the elderly.     

Self-reported health problems among Swedish miners one year after unemployment

Unemployment is considered to be a public health concern sincedeterioration in the health of the unemployed is often anticipated.However, for some groups, such as miners, unemployment mightimprove health due to a cessation of potentially harmful occupationalexposures. This study evaluates the health of 79 miners in oneSwedish iron-ore mine, and 226 age-matched controls from thegeneral population, during one year after the closure of themine. The participants received a questionnaire regarding medicalhistory and subjective symptoms at the beginning of the studyperiod, and after one year. Statistically significant negativeeffects on self-reported health attributable to unemploymentwere not found, although neuropsychiatric symptoms were morecommon among the unemployed miners. The miners reported a statisticallysignificant improvement in grip force (p=0.031). They had asignificantly higher prevalence of symptoms associated withmining related exposures when compared with the population controls;pain in the upper extremities [relative risk (RR)=2.27, 95%confidence interval (Cl)=1.44–3.59), back pain (RR=1.84;Cl=1.237–2.75), vasospastic disease of the fingers (RR=2.05;Cl=1.18–3.57) and obstructive respiratory symptoms (attacksof dyspnea and wheezing: RR=3.67; Cl=1.167–11.6).     

Excès de cas humains et animaux de tularémie en France au cours de l’hiver 2007–2008 : émergence ou phénomène isolé ?

Context

Tularemia is a zoonosis affecting humans and hares in France. We describe the results of surveillance in both species, in 2007 and 2008.

Methods

Human tularemia cases are mandatorily notifiable in France since 2003. In hares, surveillance relies on volunteer hunter associations in all districts of the country. Data from mandatory reports and volunteer surveillance in 2007/2008 were analyzed and compared with previous results.

Results

In 2007/2008, 144 cases were reported in humans and 117 cases in hares. This was a 100% increase compared to previous years. Human cases differed from those of previous years only by the frequency of contact with breeding animals. Human cases without any documented risk exposure were also more frequent.

Conclusion

An increase of tularemia cases occurred in 2007/2008 in both species. Complementary studies are needed to identify the species reservoir in France to understand the causes of this peak of cases.     

Occupational health hazards in mining: an overview

This review article outlines the physical, chemical, biological, ergonomic and psychosocial occupational health hazards of mining and associated metallurgical processes. Mining remains an important industrial sector in many parts of the world and although substantial progress has been made in the control of occupational health hazards, there remains room for further risk reduction. This applies particularly to traumatic injury hazards, ergonomic hazards and noise. Vigilance is also required to ensure exposures to coal dust and crystalline silica remain effectively controlled.     

Manufacture and use of nanomaterials: current status in the UK and global trends

This paper provides an overview of the production and use of nanomaterials (NMs), particularly in the UK. Currently, relatively few companies in the UK are identifiable as NM manufacturers, the main emphasis being the bulk markets in metals and metal oxides, and some niche markets such as carbon nanotubes and quantum dots. NM manufacturing in the UK does not reflect the global emphasis on fullerenes, nanotubes and fibres. Some assumptions have been made about the types of NM that are likely to be imported into the UK, which currently include fullerenes, modified fullerenes and other carbon-based NMs including nanotubes. Many university departments, spin-offs and private companies have developed processes for the manufacture of NMs but may only be producing small quantities for research and development (R&D) purposes. However, some have the potential to scale up to produce large quantities. The nanotechnology industry in the UK has strong R&D backup from universities and related institutions. This review has covered R&D trends at such institutions, and appropriate information has been added to a searchable database. While several companies are including NMs in their products, only a few (e.g. manufacturers of paints, coatings, cosmetics, catalysts, polymer composites) are using nanoparticles (NPs) in any significant quantities. However, this situation is likely to change rapidly. There is a need to collect more information about exposure to NPs in both manufacturing and user scenarios. As the market grows, and as manufacturers switch from the micro- to the nanoscale, the potential for exposure will increase. More research is required to quantify any risks to workers and consumers.     

深圳公立医院管理体制改革制度设计

深圳公立医院管理体制改革实行政事分开、管办分开,在理事会架构下按法定机构模式组建市医管中心,落实公立医院运营管理自主权.作者从当前公立医院管理体制的弊端入手,介绍了深圳市进行公立医院管理体制改革的基本思路及改革方案设计的主要举措,深入剖析了的改革方案的特点,并对改革效果进行了预测.     

Effects of nitrogen dioxide on red blood cells of rats: Changes in components of red cell membranes during in vivo exposure to NO2

Red cell membranes, prepared from red blood cells of rats exposed to 4, 10, or 20 ppm nitrogen dioxide (NO₂) for 1 to 10 days, were examined for evidence of changes in membrane components. Appreciable changes were not found in contents of phospholipid and cholesterol during exposure to 10 ppm NO₂. By contrast, protein content altered with the time of exposure. Moreover, changes in protein composition were observed by employing sodium dodecyl sulfate — polyacrylamide gel electrophoresis. Twenty-four-hour exposure to NO₂ at the concentration above 10 ppm resulted in a marked increase in the percentage of lysophosphatidylethanolamine (LysoPE) to the total phospholipids. The prolonged exposure to 10 ppm NO₂ gave rise to a further increase in LysoPE, whereas the percentage of phosphatidylethanolamine (PE) showed a gradual decrease. A 1-day exposure to 4.0 ppm NO₂ also caused an increase in sialic acid content and decreases in those of PE and hexose. In addition to contents of these components the percentage of LysoPE increased 5 days after exposure and the elevated values were maintained up to the end of exposure period. These results demonstrate that red blood cells in circulation exhibit different membrane properties in terms of lipid and carbohydrate composition during 10 days of exposure to 4.0 ppm NO₂.     

Investigating clusters in the workplace and beyond

Clusters of disease are common and occur in the workplace and in the general community. They often arouse considerable concern among the population. Investigations have sometimes lead to exciting new knowledge, but in general the investigation of clusters is difficult and often unrewarding, especially for community clusters. In the workplace, investigations are more likely to find associations and even new causes, but still many clusters remain enigmatic. Despite this, there are many reasons for investigating clusters, including allaying community concern and identifying uncontrolled exposures. A structure for investigating clusters in the workplace is suggested.