结核性胸膜炎患者DNA氧化损伤和脂质过氧化的研究

目的　探讨结核性胸膜炎患者单个核细胞DNA氧化损伤和脂质过氧化的程度。方法采用单细胞凝胶电泳的方法检测 2 8例结核性胸膜炎患者 (试验组 )胸腔积液和外周血单个核细胞DNA损伤及 2 5名健康人 (对照组 )外周血单个核细胞DNA损伤 (以彗星率表示 ) ;采用菲罗啉比色法检测患者胸腔积液和血浆总抗氧化能力及健康人血浆总抗氧化能力 ;硫代巴比妥酸比色法检测患者及健康人血浆丙二醛 (MDA)含量。组间差异显著性比较采用t检验。结果　试验组胸腔积液单个核细胞彗星率为 (4 1 3± 14 5 ) % ,高于其外周血单个核细胞的 (2 1 2± 4 2 ) % (P <0 0 1) ;胸腔积液总抗氧化能力为 (5 172± 1195 )U/L ,显著低于其血浆的 (86 5 6± 15 92 )U/L(P <0 0 1)。胸腔积液单个核细胞彗星率与总抗氧化能力呈负相关 (r=- 0 4 2 5 ,P <0 0 5 )。试验组外周血单个核细胞彗星率及血浆MDA含量为 (2 1 2± 4 2 ) %和 (8 2 5± 1 37) μmol/L ,分别高于对照组的 (8 9± 3 7) %和(4 4 6± 0 93) μmol/L(P均 <0 0 1) ;试验组血浆总抗氧化能力为 (86 5 6± 15 92 )U/L ,显著低于对照组的 (10 6 10± 1399)U/L (P <0 0 1)。试验组血浆总抗氧化能力分别与外周血单个核细胞彗星率、血浆MDA含量呈负相关 (r分别为 - 0 4 38、-     

用SCGE法观察砷、氟单独及联合染毒致SGC-7901细胞基因组DNA的损伤作用

目的观察砷、氟及砷氟联合染毒对SGC-7901细胞基因组DNA的损伤作用及特点.方法染毒剂量分别为10、5和1μmol/L,染毒后4 h应用单细胞凝胶电泳技术结合"彗星图像分析系统"检测DNA损伤.结果①剂量为10μmol/L和5 μmol/L时NaAsO2没有增加受累细胞的数量,增加了已受损细胞DNA的损伤程度;NaF染毒只是增加了受累细胞的数量,并没有增加受累细胞DNA的损伤程度;②氟砷联合染毒组拖尾率、尾DNA百分含量、尾长和尾动量与对照组均有显著差异,但氟与砷引起的DNA损伤作用之间没有观察到交互作用.结论 NaAsO2与NaF均可引起DNA损伤,但它们的损伤机制可能是不同的;氟与砷联合染毒仅表现为简单相加作用.     

缺锌对衰老小鼠抗氧化系统和肝脏DNA损伤修复功能的影响

目的　通过D 半乳糖诱导小鼠衰老模型 ,探讨缺锌对衰老小鼠抗氧化系统和肝脏DNA损伤与修复的影响。　方法　雄性 3月龄小鼠 70只 ,随机分成 5组 :青年组、衰老模型组、衰老缺锌组、衰老配喂组和衰老补锌组。各衰老组按 10 0mg /kg经颈背部皮下给予D 半乳糖注射液 ,青年组给予等剂量的生理盐水 ,连续 30d。衰老缺锌组和补锌组喂饲缺锌饲料 (含锌 1 6 1μg/kg) ,其他组喂饲正常锌饲料 (含锌 5 0 μg/kg) ,最后 2周补锌组喂饲补锌饲料 (10 0 μg/kg)。第 30天处死小鼠 ,取样检测血清锌、肝锌、超氧化物歧化酶、丙二醇、肝脂褐质和DNA损伤情况。　结果　与衰老模型组相比 ,衰老缺锌组血清锌 (0 5 3± 0 1)mg/L、肝锌 (14 5 4± 2 18)mg/L水平下降 ,血清和肝超氧化物歧化酶活性〔(14 2 87± 10 16 )NU/ml和 (180 11± 13 2 2 )NU/ml,P <0 0 5〕降低 ,丙二醇含量升高 ,肝脂褐质含量增高 ;彗星试验显示衰老缺锌组小鼠肝DNA损伤加重 ,彗星细胞尾长 /总长比值显著增加。补锌后上述指标均有改善。　结论　锌可有效的影响衰老的速度和程度 ,缺锌可加速衰老的进程 ,适当补锌有助于延缓衰老。     

结核性胸膜炎患者单个核细胞DNA氧化损伤及褪黑素的体外修复作用

目的通过观察结核性胸膜炎患者单个核细胞DNA氧化损伤程度、总抗氧化能力及抗氧化剂褪黑素对其的作用,评价褪黑素对结核性胸膜炎患者胸水单个核细胞DNA损伤的体外修复作用。方法用单细胞凝胶电泳检测25例健康人外周血、28例结核性胸膜炎患者胸水和外周血单个核细胞DNA损伤（以彗星率表示）,及经褪黑素处理的20例结核性胸膜炎患者胸水单个核细胞DNA损伤。用菲罗啉比色法检测健康人血浆、结核性胸膜炎患者胸水和血浆总抗氧化能力。结果健康人外周血单个核细胞彗星率为（8．9±3．7）％,血浆总抗氧化能力为（10．61±1．39）U／ml。结核性胸膜炎患者胸水单个核细胞彗星率为（41．3±14．5）％,高于其外周血[（21．2±4．2）％,P〈0．01];胸水总抗氧化能力为（5．17士1．19）U／ml,低于其血浆[（8．66±1．59）U／ml,P〈0．01]。经10p．mol／L褪黑素体外作用4h后,胸水单个核细胞彗星率由（40．8±9．3）％降至（11．0±3．7）％（f=15．251,P〈0．01）。胸水单个核细胞彗星率与总抗氧化能力呈负相关（r=-0．425,P〈0．05）。结论结核性胸膜炎患者存在DNA氧化损伤、氧化／抗氧化失衡,病变局部较全身明显。体外经褪黑素处理,能促进结核性胸膜炎患者胸水单个核细胞DNA损伤的修复,可能与其抗氧化作用有关。     

砷致昆明种小鼠基因组DNA损伤的量效关系

目的　探索砷剂量对机体DNA损伤的效应规律。方法　将体重 (2 0± 2 )g的 2 4只健康雄性昆明种小鼠随机均分为 4组 ,即Group 0 .2NaAsO2 (0 .2mg/kg体重 )、Group 0 .8NaAsO2 (0 .8mg/kg体重 )、Group 4.0NaAsO2(4mg/kg体重 )和GroupC(生理盐水对照 )。于腹腔注射药剂处理前及处理后 4,8,2 4,48h分别采集各组小鼠微量尾动脉全血进行彗星实验 ,观测指标有拖尾细胞比率、尾DNA百分含量和尾长。结果　①从细胞拖尾率指标看 ,DNA断裂损伤的程度随NaAsO2 剂量的增加而显著下降 ;②从拖尾细胞的尾部DNA碎片数量和平均尾长看 ,NaAsO2 剂量主要影响DNA分子碎片的多少而不是其长短。结论　 3价砷剂量的大小诱导不同的DNA损伤效应 ,低剂量可能以断裂为主 ,高剂量可能以交联为主。而且 ,砷致DNA分子断裂的碎片大小较恒定     

细胞黏附分子-1在急性髓性白血病细胞与内皮细胞黏附中的作用

目的　检测急性髓性白血病 (AML)细胞与内皮细胞的黏附及细胞黏附分子 1(ICAM 1)及其配体淋巴细胞功能相关抗原 1(LFA 1)在黏附中的作用。方法　观察AML细胞与静止内皮细胞和肿瘤坏死因子α(TNFα)激活的内皮细胞的黏附 ;AML细胞与内皮细胞混合培养 2 4h的黏附 ;正常中性粒细胞与AML细胞培养上清作用 2 4h后的内皮细胞的黏附 ;流式和ELISA方法检测AML细胞培养上清作用后内皮细胞ICAM 1及可溶性ICAM 1的表达 ;并用ICAM 1和LFA 1的抗体进行阻滞黏附试验。结果　AML细胞与静止的内皮细胞黏附较少 (2 4 33± 2 87) % ,AML细胞与TNFα激活的内皮细胞的黏附 ,与内皮细胞混合培养 2 4h后的黏附以及正常中性粒细胞与AML细胞培养上清作用后内皮细胞的黏附明显增加 ,分别为 (81 87± 4 0 8) % ,(82 0 6± 7 0 5 ) % ,(83 99± 3 86 ) % (n =2 1,P <0 0 0 1) ;静止的内皮细胞ICAM 1及可溶性ICAM 1的表达分别为 (5 5 81± 4 11) %和 (0 839± 0 2 36 )μg/L ;AML细胞培养上清作用后内皮细胞ICAM 1及可溶性ICAM 1的表达明显增加 ,分别为 (6 5 36±5 97) %和 (1 4 2 4± 0 4 6 9) μg/L(n =2 1,P <0 0 5 ) ;用ICAM 1及LFA 1的抗体进行黏附阻滞后 ,AML细胞与TNFα激活的内皮细胞的黏附下降为 (2 0 12±     

四氢喋呤对兔缺血再灌注损伤内皮功能的保护作用

目的　研究四氢喋呤 (BH4 )对兔实验性缺血再灌注 (MI R)损伤中一氧化氮 (NO)、丙二醛 (MDA)、超氧化物歧化酶 (SOD)水平及心肌梗死面积的影响。方法　 2 4只新西兰兔随机分为假手术组、模型组和药物干预组 3组。制备MI R模型 ,观察BH4 预处理后MI R损伤中NO、MDA、SOD水平的变化及对心肌梗死面积的影响。结果　模型组较假手术组NO显著减低 [(2 8± 10 ) μmol L比(116± 17) μmol L ,P <0 0 1],MDA水平明显升高 [(5 8 3± 10 4 )nmol L比 (7 0± 1 8)nmol L ,P <0 0 1],SOD活性明显减低 [(2 6 8± 17)nu ml比 (340± 2 4 )nu ml,P <0 0 5 ];而BH4 预处理组较模型组NO明显升高 [(6 2± 17) μmol L比 (2 8± 10 ) μmol L ,P <0 0 1],MDA明显减低 [(30 9± 6 1)nmol L比(5 8 3± 10 4 )nmol L ,P <0 0 1],SOD活性无明显改变 [(2 88± 2 0 )nu ml比 (2 6 8± 17)nu ml,P >0 0 5 ];BH4 预处理组和模型组心肌梗死面积差异有显著性 [(18± 4 ) %比 (16± 4 ) % ,P <0 0 5 )。结论　MI R导致内皮功能紊乱。BH4 对内皮功能有保护作用 ,从而减轻再灌注损伤。     

砷与5-氮胞苷对人淋巴细胞DNA损伤的联合作用

为探讨砷和5－氮胞苷对人淋巴细胞DNA损伤及修复的联合作用，应用单细胞凝胶电泳（SCGE）技术比较研究了5－氮胞苷与砷同时和前后作用于人类淋巴细胞产生的联合毒性，结果显示10μmol/L5-氮胞苷和10μmol/L砷单独处理人淋巴细胞2h引起明显的DNA泳动（彗星尾），但两试剂引起的DNA泳动（彗星尾）间无显差异，5－氮胞苷前处理与砷后处理2h引起的彗星尾与其单独处理组比较非常显，砷前处理与5－氮胞苷后处理引起的彗星尾与其单独处理组比较无显性差异，但较对照组差异显，10μmol/L5-氮胞苷和10μmol/L砷分别单独处理2h引起了人淋巴细胞显的DNA损伤（链断裂），5－氮胞苷与砷在对淋巴细胞DNA的损伤上表现为单纯相加作用。5－氮胞苷前处理显增加了细胞对砷的基因毒性的敏感性，或砷后处理显增加了5－氮胞苷引起的DNA损伤，5－氮胞苷后处理2h显抑制了细胞对砷所致DNA损伤的修复。     

冠心病患者血浆氧化低密度脂蛋白和同型半胱氨酸与循环内皮细胞和内皮素相关性研究

目的　通过对 58例冠心病患者血浆中循环内皮细胞、内皮素、氧化低密度脂蛋白和同型半胱氨酸水平的观察 ,探讨它们与动脉粥样硬化发生过程中的关系 ,以及氧化低密度脂蛋白和同型半胱氨酸与循环内皮细胞和内皮素之间的相关性。方法　分别用酶联免疫吸附法和高效液相色谱分析法测定血浆中氧化低密度脂蛋白和同型半胱氨酸水平 ,同时测定血浆中循环内皮细胞和内皮素水平 ,进行对比和直线相关性分析。结果　冠心病组循环内皮细胞 :(7 78± 3 31 )cells/ 0 9μl,内皮素(98 1 4± 35 0 8)ng/L ,氧化低密度脂蛋白 (80 9 2 5± 31 1 89) μg/L ,同型半胱氨酸 (1 9 40± 7 0 3) μmol/L。对照组上述指标分别为 :(4 1 0± 1 60 )cells/ 0 9μl,(52 61± 1 5 71 )ng/L ,(438 2 4± 2 0 0 54) μg/L和(1 1 1 9± 2 94) μmol/L。两组比较P均小于 0 0 0 1。冠心病组氧化低密度脂蛋白与血浆循环内皮细胞、内皮素均呈正相关 ,相关系数分别为 0 92 6(P <0 0 0 1 )、0 979(P <0 0 0 1 ) ,同型半胱氨酸同样与循环内皮细胞、内皮素呈正相关 ,相关系数分别为 0 947(P <0 0 0 1 )、0 90 0 (P <0 0 0 1 ) ,且冠心病组血浆循环内皮细胞和内皮素呈正相关 ,相关系数为 0 939(P <0 0 0 1 )。结论　氧化低密度脂     

西立伐他汀对血管内皮细胞一氧化氮合酶及细胞间黏附分子的作用

目的　观察西立伐他汀对内皮细胞一氧化氮合酶 (NOsythase ,eNOS)和细胞间黏附分子 1 (intercellularadhesionmolecule 1 ,ICAM 1 )基因的表达 ,NOS活力和黏附的THP 1细胞量的影响。方法　以氧化LDL抑制培养的ECV 3 0 4细胞表达eNOS ,加入不同浓度西立伐他汀后 ,用RT PCR法检测eNOSmRNA ,硝酸还原酶法测定培养基中NO量。以脂多糖 (LPS)及西立伐他汀加入ECV 3 0 4细胞后 ,用RT PCR法检测ICAM 1mRNA ,并测定黏附的THP 1细胞量。结果　随着西立伐他汀浓度增加 ,内皮细胞eNOSmRNA水平增加 ,0 0 1 ,0 1 ,1 0 μmol/L时分别增加 5 0 %,1 5 0 %,3 0 0 %,P均 <0 0 5。培养液中NO亦相应增加 ,0 0 1 ,0 1 ,1 0 μmol/L时分别增加 2 6 7%,92 3 %,2 3 0 %,P <0 0 5。西立伐他汀浓度为 0 1 ,1 0 μmol/L时 ,ICAM 1mRNA分别从 70 7± 1 0 4降至 5 6 2± 6 5 ,3 5 8± 4 2 ,P <0 0 5。黏附于ECV 3 0 4细胞的THP 1细胞在 1 0 μmol/L时被抑制 2 6 %,P <0 0 5。结论　西立伐他汀能诱导内皮细胞eNOS基因的表达及增加NOS活力 ;抑制内皮细胞表达ICAM 1mRNA及THP 1细胞黏附于内皮细胞     

Three layer functional model and energy exchange concept of aging process

Relying on a certain degree of abstraction, we can propose that no particular distinction exists between animate or living matter and inanimate matter. While focusing attention on some specifics, the dividing line between the two can be drawn. The most apparent distinction is in the level of structural and functional organization with the dissimilar streams of ‘energy flow’ between the observed entity and the surrounding environment. In essence, living matter is created from inanimate matter which is organized to contain internal intense energy processes and maintain lower intensity energy exchange processes with the environment. Taking internal and external energy processes into account, we contend in this paper that living matter can be referred to as matter of dissipative structure, with this structure assumed to be a common quality of all living creatures and living matter in general. Interruption of internal energy conversion processes and terminating the controlled energy exchange with the environment leads to degeneration of dissipative structure and reduction of the same to inanimate matter, (gas, liquid and/or solid inanimate substances), and ultimately what can be called ‘death.’ This concept of what we call dissipative nature can be extended from living organisms to social groups of animals, to mankind. An analogy based on the organization of matter provides a basis for a functional model of living entities. The models relies on the parallels among the three central structures of any cell (nucleus, cytoplasm and outer membrane) and the human body (central organs, body fluids along with the connective tissues, and external skin integument). This three-part structural organization may be observed almost universally in nature. It can be observed from the atomic structure to the planetary and intergalactic organizations. This similarity is corroborated by the membrane theory applied to living organisms. According to the energy nature of living matter and the proposed functional model, the decreased integrity of a human body's external envelope membrane is a first cause of the structural degradation and aging of the entire organism. The aging process than progresses externally to internally, as in single cell organisms, suggesting that much of the efforts towards the restoration and maintenance of the mechanisms responsible for structural development should be focused accordingly, on the membrane, i.e., the skin. Numerous reports indicate that all parts of the human body, like: bones, blood with blood vessels, muscles, skin, and so on, have some ability for restoration. Therefore, actual revival of not only aging tissue of the human body's membrane, but the entire human body enclosed within, with all internal organs, might be expected. We assess several aging theories within the context of our model and provide suggestions on how to activate the body's own anti-aging mechanisms and increase longevity. This paper presents some analogies and some distinctions that exist between the living dissipative structure matter and inanimate matter, discusses the aging process and proposes certain aging reversal solutions.     

Unusual responses of nocturnal pineal melatonin synthesis and secretion to swimming: Attempts to define mechanisms

Abstract: The effect of swimming at night on rat pineal melatonin synthesis was compared with that of light exposure at night. Rats were forced to swim at 0030 hr (lights out at 2000 hr) and sacrificed by decapitation 15 and 30 min later, immediately after swimming. Other groups of animals were exposed to white light (650μW/cm²) for 15 and 30 min at same time. Swimming caused a rapid and highly significant drop in the melatonin content in the pineal gland; however, the activity of N-acetyltransferase (NAT), the supposed rate limiting enzyme in the melatonin production, was not changed. Despite the drop in pineal melatonin levels, serum concentrations of the indole remained elevated in the rats that swam. In contrast, melatonin levels in the pineal and serum of light exposed rats fell precipitously, accompanied by a significant suppression of NAT activity. Since we anticipated that the strenuous exercise associated with swimming may induce release of artrial natriuretic peptide (ANP) from the heart, which in turn could cause the release of pineal melatonin, in a second study we injected physiological saline intravenously to stretch the cardiac muscle and release ANP. Three milliliters of normal saline was injected during the day into the jugular vein of anesthetized rats that were pretreated with isoproterenol to stimulate pineal melatonin production. Animals were killed 15 min after the saline injection, and pineal NAT activity and pineal melatonin levels were measured. The saline injections caused no alteration in the elevated levels of either NAT or melatonin. These data suggest that the disparity in pineal NAT activity (which was high) and pineal melatonin (which was low), in animals swum at night, may not be caused by ANP which is released during strenuous exercise such as swimming.     

The immunoneuroendocrine role of melatonin

Abstract: A tight, physiological link between the pineal gland and the immune system is emerging from a series of experimental studies. This link might reflect the evolutionary connection between self-recognition and reproduction. Pinealectomy or other experimental methods which inhibit melatonin synthesis and secretion induce a state of immunodepression which is counteracted by melatonin. In general, melatonin seems to have an immunoenhancing effect that is particularly apparent in immunodepressive states. The negative effect of acute stress or immunosuppressive pharmacological treatments on various immune parameters are counteracted by melatonin. It seems important to note that one of the main targets of melatonin is the thymus, i.e., the central organ of the immune system. The clinical use of melatonin as an immunotherapeutic agent seems promising in primary and secondary immunodeficiencies as well as in cancer immunotherapy. The immunoenhancing action of melatonin seems to be mediated by T-helper cell-derived opioid peptides as well as by lymphokines and, perhaps, by pituitary hormones. Melatonin-induced-immuno-opioids (MHO) and lymphokines imply the presence of specific binding sites or melatonin receptors on cells of the immune system. On the other hand, lymphokines such as -γ-interferon and interleukin-2 as well as thymic hormones can modulate the synthesis of melatonin in the pineal gland. The pineal gland might thus be viewed as the crux of a sophisticated immunoneuroendocrine network which functions as an unconscious, diffuse sensory organ.     

Melatonin and photoperiodic time measurement: Seasonal breeding in the sheep

Abstract: Well-established circadian physiology supports the view that photoperiodic time measurement utilizes the coincidence between the presence of light and a photosensitive phase of a 'biological clock' to alter reproductive status—the so-called external coincidence model of seasonal breeding. In this review, we examine the mechanism whereby photoperiod interacts with presumed suprachiasmatic nuclei activity to allow endogenous melatonin to normally synchronize reproductive activity to the optimal time of year. The Romney Marsh sheep is particularly explored as an experimental model. It is suggested that the on/off activity of seasonal reproduction may be a robust mechanism able to be predictably manipulated by the judicious use of the light/dark cycle and exogenous melatonin, but firmly based on circadian principles.     

Response of rat pineal melatonin to calcium, magnesium, and lithium is circadian stage dependent

Abstract: Herein we documented the response of pineal melatonin production to electrolytes known to be effective on pineal function in view of a possible circadian stage dependence. We studied the release of melatonin by perifused rat pineal glands at 2 different circadian stages corresponding to the middle of the light and dark periods, i.e., respectively, 7 and 19 HALO (Hours After Light Onset, L:D = 12:12). The initial efflux rates were, as expected, much higher in the perifusates of glands removed from rats sacrificed during the dark phase than of those removed during the light phase. After 3 hr of perifusion, melatonin release reached similar levels which were found constant up to the 8th hr of perifusion, whatever the circadian stage. Perifusion of the glands with physiological concentrations for the rat of calcium (5.2 mmol/1) and magnesium (1.34 mmol/1) resulted in a stimulatory effect on the pineal glands removed from rats sacrificed in the middle of the dark period (19 HALO), whereas no effects were observed on the pineal glands removed from rats sacrificed during the light (7 HALO). Lithium (0.28 and 0.55 mmol/1) was ineffective on melatonin release in pineal glands removed 7 and 19 HALO. Our results show differences in the initial efflux rates of melatonin and in the response of perifused pineal glands to calcium and magnesium according to the circadian stage.     

Conservative management of perforated duodenal diverticulum： A case report and review of the literature

Duodenal diverticula are a relatively common condition. They are asymptomatic, unless they become complicated, with perforation being the rarest but most severe complication. Surgical treatment is the most frequently performed approach. We report the case of a patient with a perforated duodenal diverticulum, which was diagnosed early and treated conservatively with antibiotics and percutaneous drainage of secondary retroperitoneal abscesses. We suggest this method could be an acceptable option for the management of similar cases, provided that the patient is in good general condition and without septic signs.     

Changes in connexin43, the gap junction protein of astrocytes, during development of the rat pineal gland

Abstract: The abundance of gap junctions between rat pineal astrocytes formed by connexin43 (Cx43) was studied during development. Levels and distribution of Cx43 were measured by immunoblotting and indirect immunofluorescence, respectively. The amount of Cx43 in cells located within the gland was low until about the 7th postnatal day and increased to adult values between the 14th and 21st days postpartum. Although astrocytes, recognized by their vimentin immunoreactivity, were scarce before birth, they were abundant by the 7th postnatal day suggesting that the low levels of Cx43 found at this age corresponded to a low expression of this protein. Localization of the immunoreactivity to Cx43 and vimentin showed a close correlation, indicating that mature or immature pineal astrocytes form gap junctions made of Cx43. Since Cx43 levels attained their adult values at about the time the innervation and the functional state of the gland reached maturity (2–3 weeks after birth), it is proposed that astrocyte gap junctions are involved in the function of the adult rat pineal gland.     

Language of CTO interventions – Focus on hardware

The knowledge of variety of chronic total occlusion (CTO) hardware and the ability to use them represents the key to success of any CTO interventions. However, the multiplicity of CTO hardware and their physical character and the terminology used by experts create confusion in the mind of an average interventional cardiologist, particularly a beginner in this field. This knowledge is available but is scattered. We aim to classify and compare the currently used devices based on their properties focusing on how physical character of each device can be utilized in a specific situation, thus clarifying and simplifying the technical discourse.