血清CK、CK—MB、cTnI对婴幼儿患者心肌损害诊断的临床研究

目的探讨婴幼儿患者血清、CK—MB及cTnI对心肌损害的诊断价值。方法对196例和102例心电图和临床表现有、无心肌损害表现的婴幼儿患者和正常对照儿童进行血清CK、CK—MB及cTnI测定。结果有心肌损害组三项指标分别为CK（236．2±127．2）U／L;CK—MB（32．2±12．7）U／L;cTnI（0．24±0．13）ng／ml,均明显高于无心肌损害表现组及正常对照组（P〈0．01）,但特异性和敏感性却不尽相同,联合检验的敏感性及准确性达93．4％和80．5％,均有显著提高（P〈0．05）。结论血清CK、CK—MB及cTnI在对婴幼儿患者心肌损害反映中,CK、CK—MB特异性不高,同时要考虑到单纯CK、CK—MB活性增高可能是生理、标本和试剂等因素所致,不具有临床诊断价值;cTnI特异性最高,但在心肌轻度损害时敏感性不高;因此诊断婴幼儿患者心肌损害时应联合这三项并结合心电图和临床表现来综合确定诊断。     

CK—MB与CK比率界值在鉴别心肌梗死与骨骼肌损伤中的应用

目的探讨CK-MB/CK比值鉴别诊断急性心肌梗死(简称心梗)和肌损伤的可行性.方法采集心梗患者和肌损伤患者的肌酸激酶(CK)、肌酸激酶MB同工酶(CK-MB)资料,进行显著性分析,确定不同诊断界值后分别计算敏感性、特异性和诊断指数.在分析比较的基础上,最后确定鉴别诊断的比率界值.结果心梗患者CK对数均值为617(162～3495)u/L,肌损伤组为589(165～5452)u/L,两组比较无显著性差异(t=1.74,P＞0.05).CK-MB心梗组对数均值高于肌损组,分别为68(9～530)u/L和24(8～183)u/L,t=5.83,P＜0.01,但总体诊断指数小于150%.CK-MB/CK比值,心梗组均值亦高于肌损组,分别为(11.4±4.08)%和(4.47±2.07)%,t=11.17,P＜0.01.将比率界值定为6%,其诊断指数可达176%,优于CK-MB峰值的诊断效率.结论以CK-MB/CK比率界值作为鉴别诊断心梗和肌损伤的指标是可行的,同时提出了用CK、CK-MB诊断心梗的4条标准.     

203例新生儿高胆红素血症对心肌酶CK、CK—MB活性影响的临床研究

目的：探讨新生儿高胆红素血症对心肌酶活性的影响,以及与心肌损害的关系。方法：203例新生儿高胆红素血症作为治疗组,130例同期出生的正常新生儿作为对照组。监测两组治疗前后的心肌酶CK、CK—MB值。结果：胆红素含量越高,心肌酶活性也高。治疗组治疗前后心肌酶谱值比较,差异有统计学意义（P〈0．05）。结论：临床儿科医生在治疗新生儿黄疸患儿时,应将心肌酶谱列为常规检查项目,避免新生儿黄疸患儿因心肌损害而死亡。     

病毒性心肌炎患者血清CK—MB检测的临床意义

我们采用逐步回归的方法分析了病毒性心肌炎患儿血清肌酸激酶心型同功酶(CK MB)检测的临床意义,现将结果报告如下。1 临床资料 1.1 对象 1993～1996年住院的病毒性心肌炎患儿53例,其中男26例,女27例;年龄最小3岁,最大15岁。采血时病程:最短发病当天,最长31天。     

血清肌酸激酶及CK—MB同功酶测定的临床意义

67例健康成人用金氏法测得血清 CK 参考值为31.7±19.5U/L,用动力学方法测得20例健康成人 CK-MB 参考值为13.1±6.8U/L(37℃)。对10例 AMI 患者作了观察,发现 AMI后,CK-MB/CK 比值开始升高时间较 CK 为早,在4小时以内都超过6%,该比值从高逐渐降至正常,为最感敏的指标。以方法学而论,则动力学方法较比色法敏感。本文还讨论了 CK 及CK-MB 同功酶测定的临床应用。     

异氟醚对非体外循环冠脉搭桥手术患者CK、CK—MB及cTnI的影响

目的：观察异氟醚对非体外循环冠脉搭桥患者肌酸激酶（creatine kinase,CK）、肌酸激酶同工酶（creatine kinase—MB,CK—MB）以及心肌肌钙蛋白I（cardiac troponin I,cTnI）的影响,探讨其心肌保护作用机制。方法：将42例非体外循环冠脉搭桥患者随机分为异氟醚组和丙泊酚组,每组各21例。分别于术前、术后6h、术后12h和术后24h抽取静脉血,测定CK、CK—MB和cTnI。结果：两组术前CK比较,差异无统计学意义。异氟醚组CK于术后6h、术后12h和术后24h分别低于丙泊酚组（P〈0．01）。两组术前CK—MB比较,差异无统计学意义。异氟醚组CK-MB于术后6h、术后12h和术后24h分别低于丙泊酚组（P〈0．01）。两组术前cTnI比较,差异无统计学意义。异氟醚组cTnI于术后6h、术后12h和术后24h均低于丙泊酚组（P〈0．01）。结论：异氟醚可降低非体外循环冠脉搭桥患者CK、CK—MB和cTnI的释放。是一种安全有效的麻醉药物。     

早期急性心肌梗死患者cTnI和hs—CRP及CK—MB测定的临床意义

目的 研究早期心肌梗死患者特异性指标的变化。方法选取56例急性心肌梗死（AMI）患者作为研究组,健康体检者30例作为对照组,检测2组肌钙蛋白Ⅰ、高敏C-反应蛋白（hs-CRP）和肌酸激酶同工酶（CK-MB）的水平。结果研究组心肌肌钙蛋白（cTn）、hs-CRP和CK—MB水平与对照组比较差异有统计学意义（P〈0．01）。结论AMI患者cTnI,hs-CRP和CK-MB联合检测对AMI的诊断、危险评估具有重要意义。     

68例新生儿窒息后心肌损害血清CK—MB变化

肌酸磷酸激酶 (ＣＫ )的同工酶ＣＫ ＭＢ是反映心肌细胞损害的特异性较高的血清酶 ,临床上用于诊断新生儿窒息后心肌损害 ,但一些非窒息后心肌损害患儿的血清中亦见增高 ,为探讨血清心肌酶谱学检查的临床意义 ,本文将 1992年～ 1998年来收治的 68例新生儿窒息后心肌损害患儿血清中ＣＫ ＭＢ变化报告如下。临床资料一、一般资料　选择窒息后心肌损害住院的新生儿 ,所有病例均符合Ａｐｇａｎ评分诊断标准 ,男 58例 ,女 10例。日龄 :发病在 2 4小时内 30例 ,36小时 2 5例 ,4 8小时 13例。入院后均作血气分析 ,动脉血氧分压 (ＰａＯ2 )在 5 5～ …     

Anti-uveitis and inhibition of fibroblast-like corneal and conjunctival cells by interleukin-1 blockers

Effects of interleukin-1 (IL-1) blockers, CK130 and CK131, on IL-1-induced uveitis and proliferation of fibroblast-like corneal and conjunctival cells were investigated in this study. It was found that CK130 and CK131 inhibited IL-1-induced uveitis in rat eyes effectively at 3 mg/kg and 10 mg/kg, respectively. Further, CK130 and CK131 inhibited fibroblast-like corneal and conjunctival cell growth effectively at 10–300 μg/ml and 30–300 μg/ml, respectively. It was also found that DNA synthesis was markedly reduced by CK130 and CK131 at 30–100 μg/ml. RNA synthesis was also inhibited by these CK compounds but protein synthesis was little affected or enhanced.     

General pharmacology of CK-2130: A new selective positive inotrope

CK-2130 is a new imidazolone developed to treat congestive heart failure. We compared CK-2130 to four inodilators and ouabain in several pharmacologic models. Intravenous (i.v.) administration of CK-2130 to pentobarbital-anesthetized dogs (0.03 to 1 mg/kg) relatively selectively increased myocardial dP/dT when compared to the dual positive inotropic and vasodilator activity of milrinone, enoximone, imazodan, and piroximone. Milrinone and piroximone (600 mg/kg, p.o., and 30-300 mg/kg, i.p.) were central nervous system depressants in mice. CK-2130 (100 mg/kg, i.v. and 600 mg/kg, i.p. and p.o.) was not depressant. Gastric acid secretion in the guinea pig was not affected by CK-2130 (1 mg/kg, i.v.) and was inhibited by milrinone (1 mg/kg, i.v.) and enhanced by enoximone (1 mg/kg, i.v.). CK-2130 and milrinone (0.03-1 mg/kg, i.v.) did not affect rabbit sciatic nerve-gastrocnemius muscle function. CK-2130, piroximone, imazodan, and milrinone (100 μM) did not affect sympathetic neurotransmission, postsynaptic receptors, or guinea-pig nonvascular smooth muscles but relaxed canine arteries and veins. Ouabain (1-100 μM) initially facilitated, then inhibited, sympathetic neurotransmission, contracted vascular and non-vascular smooth muscles, enhanced the vas deferens contraction to norepinephrine, and inhibited uterine contractions to bradykinin (10 μM). CK-2130, milrinone, piroximone, and imazodan (0.1 to 100 μM) inhibited human platelet aggregation produced by adenosine diphosphate and sodium arachidonate. Thus, CK-2130, a relatively selective positive inotrope, should be devoid of adverse central nervous system; neural, smooth, and skeletal muscle; and gastrointestinal side effects associated with digitalis and enoximone therapy.     

肝素对生长因子诱导的大鼠肺动脉平滑肌细胞分裂和增殖的影响

目的：探讨肝素是否能抑制生长因子诱导的大鼠肺动脉平滑肌细胞（ＰＡＳＭＣ）分裂和增殖。方法：应用含１０％ＦＢＳ的Ｍ－１９９培养液培养大鼠ＰＡＳＭＣ。细胞分裂及细胞增殖分别用［ｍｅｔｈｙｌ－＾３Ｈ］ＴｄＲ和细胞计数监测。结果：ＦＢＳ（１０％），以及ＦＢＳ（１％）与ＰＤＧＦ（５０μｇ·Ｌ＾－１），ＦＧＦ（５０μｇ·Ｌ＾－１），或ＩＬ－１α（１００ｎｇ·Ｌ＾－１）联合应用均能增加大鼠ＰＡＳＭＣ分裂。肝素（     

Synthesis and cytotoxic action of 1-oxoalkyl and 1,2-dioxoalkyl-1,2,4-triazolidine-3,5-diones in murine and human tissue cultured cells.

1-Oxoalkyl and 1,2-dioxoalkyl-1,2,4-triazolidine-3,5-diones proved to be potent antineoplastic agents in mouse tumors and potent cytotoxic agents particularly against the growth of suspended tumor cells. The compounds with shorter substituents in position 1 or positions 1 and 2 afforded the better activity. In L1210 lymphoid leukemia cells DNA, RNA, and protein syntheses were inhibited at 100 microM after 60 min. Multiple enzyme sites in nucleic acid metabolism were affected by the compounds, i.e. DNA polymerase alpha, PRPP-amido transferase, dihydrofolate reductase, thymidylate synthetase, and nucleoside kinases. These effects of the agents are probably additive in bringing about inhibition of DNA synthesis and cell death.     

AG490对肾小管上皮细胞转分化影响的实验研究

目的探讨炎症介质的特异性阻断剂AG490在白介素-1β(interleukin-1βIL-1β)诱导的高糖培养的人肾小管上皮细胞转分化中的作用。方法体外培养人肾近曲小管上皮细胞株(HKCs),随机分为高糖对照组(30mmol·L-1);高糖(30mmol·L-1)+IL-1β(5μg·L-1)组;高糖(30mmol·L-1)+IL-1β(5μg·L-1)+AG490(10μmol·L-1)组。分别于处理后24、48、72h收集细胞,采用免疫细胞化学染色和蛋白Western blot法检测细胞角蛋白-18(cytokeratin-18,CK-18)、α-平滑肌肌动蛋白(α-smooth muscle actin,α-SMA)水平。结果IL-1β能使高糖培养的人肾小管上皮细胞α-SMA蛋白的合成增加,而肾小管上皮细胞的标志物CK-18的表达逐渐减少;IL-1β刺激的同时加入AG490干预能减弱IL-1β对肾小管上皮细胞α-SMA蛋白的诱导作用,并使CK-18的表达回升。结论炎症因子IL-1β能促进高糖培养的HKC发生表型转化,而炎症特异性阻断剂AG490能部分阻断IL-1β的该作用。     

5-Chloro-7-iodo-8-hydroxyquinoline (clioquinol) inhibits the nerve growth factor-induced stimulation of RNA synthesis in neonatal rat superior cervical ganglion, in vitro--comparison with effects of methylmercuric chloride and 4-hydroxyaminoquinoline-N-oxide

The inhibitory effects of 5-chloro-7-iodo-8-hydroxy-quinoline (clioquinol), methylmercuric chloride and 4-hydroxyaminoquinoline-N-oxide(4-HAQO) on DNA, RNA and protein syntheses in the neonatal rat superior cervical ganglion (SCG) were studied in relation to the action of mouse 2.5S nerve growth factor (NGF), using organ cultures. RNA and protein syntheses in SCG were stimulated approximately 3- and 2-fold, respectively, by NGF (1 microgram/ml), but the DNA synthesis was only slightly or not at all stimulated. Methylmercuric chloride and 4-HAQO dose-dependently inhibited DNA, RNA and protein syntheses, either in the presence or in the absence of NGF. On the other hand, clioquinol (up to 100 microM) slightly or not at all inhibited RNA synthesis in the absence of NGF; however, it did abolish the NGF-induced stimulation of RNA synthesis in the presence of NGF. The DNA and protein syntheses were dose-dependently inhibited by clioquinol, either in the presence or in the absence of NGF. We conclude from this study that the interaction between clioquinol and the functions of NGF raises the question of a possible toxicity of the drug on specific neurons.     

丝裂霉素或顺铂对离体淋巴因子激活的杀伤细胞增殖和抗膀胱癌细 …

AIM: To study the effect of mitomycin (Mit) or cisplatin (Cis) on the proliferation of lymphokine-activated killer (LAK) cells in patients with transitional cell cancer of bladder and their cytolysis to bladder tumor cells. METHODS: LAK cell proliferation was assayed in the presence of Mit or Cis by cell counting. Bladder cancer cell lines BIU-87 and EJ were cultured as target cells and cytotoxicity of LAK cells was determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. RESULTS: The proliferation of LAK cells induced by recombinant interleukin-2 (IL-2) was inhibited by Cis in a concentration-dependent manner and was decreased to 55.3% at 100 mg.L-1 compared with control at 96 h. The enhanced growth of the LAK cells was observed with Mit 5-10 mg.L-1 from 48 to 96 h. Cis 10 mg.L-1 increased the cytotoxicity against BIU-87 and EJ cells. CONCLUSION: Immunomodulatory effect of chemotherapeutic agents on LAK cell proliferation induced by IL-2 in patients with bladder cancer mainly depends on the drug itself.     

Evaluation of 1-(3,4-dichlorophenyl)-4-dimethylaminomethyl-1-nonen-3-one hydrochloride effect on nucleic acid and protein syntheses using murine leukemia L-1210 cells

Several Mannich bases derived from conjugated styryl ketones were shown to have potent cytotoxicity toward murine leukemia L-1210 cells and Walker 256 carcinosarcoma cells in culture. The most cytotoxic derivative, (E)-1-(3,4-dichlorophenyl)-4-dimethylaminomethyl-1-nonen-3-one hydrochloride, profoundly inhibited the incorporation of tritiated leucine into protein(s) and tritiated deoxythymidine into DNA at concentrations of 0.79-1.32 muM in L-1210 cells. At higher concentrations, incorporation of triated uridine into RNA and tritiated deoxyuridine into DNA was inhibited to a lesser degree. This compound failed to inhibit the enzymes thymidylate synthetase or dihydrofolate reductase up to a concentration of 10-4 M and was ineffective in retarding the growth of the Walker 256 carcinosarcoma in rats.     

吲哚美辛对脂多糖引起的人类风湿性关节炎滑膜细胞中白介素-6表达的影响

目的研究吲哚美辛对脂多糖引起的人类风湿性关节炎（RA）成纤维状滑膜细胞(FLS)中白介素-6（IL-6）表达的影响。方法用放免分析法检测IL-6蛋白的表达水平； RT-PCR方法测定IL-6 mRNA的表达水平。结果LPS处理对FLS中IL-6表达无显著影响； LPS刺激的U937细胞培养液上清液可明显增强FLS 中IL-6蛋白分泌及mRNA表达； 吲哚美辛可显著抑制上述变化，且其抑制作用随浓度的增加而增强。结论吲哚美辛可抑制LPS刺激的U937细胞培养上清液引起的FLS中IL-6的表达。     

Interleukin-1alpha and tumour necrosis factor-alpha modulate airway smooth muscle DNA synthesis by induction of cyclo-oxygenase-2: inhibition by dexamethasone and fluticasone propionate

1. Previous studies have established that glucocorticoids inhibit airway smooth muscle DNA synthesis. The effects of a combination of the pro-inflammatory cytokines, interleukin-1alpha (IL-1alpha) and tumour necrosis factor-alpha (TNF-alpha) on the inhibition of DNA synthesis by glucocorticoids in human cultured airway smooth muscle have now been investigated, since these cytokines are chronically expressed in asthmatic airways. 2. Thrombin (0.3 u ml(-1)) and basic fibroblast growth factor (bFGF, 300 pM) stimulated increases in DNA synthesis which were concentration-dependently inhibited by dexamethasone (1-1000 nM). 3. The cytokine mixture, comprising IL-1alpha (0.01 and 0.1 pM) and TNF-alpha (3 and 30 pM), directly evoked increases in DNA synthesis which were attenuated by dexamethasone. However, the cytokine mixture prevented responses to bFGF or thrombin. 4. Paradoxically, in the presence of the cytokine mixture and bFGF, dexamethasone (1-1000 nM) concentration-dependently increased DNA synthesis. Furthermore, neither dexamethasone (100 nM) nor fluticasone propionate (1 nM) inhibited DNA synthesized in response to bFGF/cytokine mixture combination and dexamethasone was similarly inactive against the thrombin/cytokine mixture. 5. The levels of prostaglandin E2 (PGE2), an established inhibitor of airway smooth muscle DNA synthesis, remained below the limits of assay detection (0.05 nM) under basal conditions or following stimulation with either thrombin or bFGF. In contrast, the cytokine mixture alone, and in the presence of thrombin or bFGF, induced biologically active levels of PGE2. Dexamethasone (100 nM), the non-selective cyclo-oxygenase (COX) inhibitor indomethacin (3 microM) or the selective COX-2 inhibitor L-745,337 (0.3 microM) completely inhibited synthesis of PGE2. 6. Neither indomethacin (3 microM) nor L-745,337 (0.3 microM) influenced thrombin- or bFGF-induced DNA synthesis. However, each COX inhibitor enhanced DNA synthesis in cytokine-treated cells. 7. In unstimulated airway smooth muscle cells, COX-1, but not COX-2 protein was detectable by Western blotting. The induction of COX-2 protein by the cytokine mixture was attenuated by dexamethasone (100 nM), whereas the level of COX-1 protein was unaffected by either the cytokines or by dexamethasone. 8. Cytokine-induced, COX-2-dependent eicosanoid production inhibits DNA synthesis. The paradoxical increase in DNA synthesis observed in glucocorticoid treated airway smooth muscle stimulated by cytokine/bFGF combinations may be explained by the ability of glucocorticoids to repress COX-2 induction and prevent cytokine-induction of the DNA synthesis inhibitor, PGE2.