血清CA153、CA125和CEA联合检测在乳腺癌诊断中的应用

目的探讨检测外周血肿瘤标志物CA153、CA125和CEA在乳腺癌的临床应用价值。方法应用电化学发光技术检测20例健康对照者、55例乳腺癌患者以及20例乳房良性肿瘤患者手术前、后血清中CA153、CA125和CEA含量。结果乳腺癌患者组血清CA153、CA125、CEA含量较健康对照组显著升高（P〈0．05）,其中CEA和CA153含量较乳房良性肿瘤患者组显著升高（P〈0．05）。手术后,患者血清中CA153含量较手术前明显下降,差异具有统计学意义（P〈O．05）。临床分期为Ⅲ、Ⅳ期的乳腺癌患者外周血CEA和CA153含量较健康对照组显著升高（P〈0．05）;Ⅲ、Ⅳ期的乳腺癌患者外周血CA153含量较Ⅰ、Ⅱ期患者显著升高（P〈0．05）。联合检测CA153、CA125、CEA,敏感性达53．8％,特异性为83．3％。结论检测CA153、CA125、CEA对乳腺癌的诊断有一定的价值,其中CA153和CEA对良、恶性乳腺肿瘤的鉴别诊断、乳腺癌病情进程的监测有实用价值。     

检测CA199、CA125、CA153及CEA在肿瘤诊断中的意义

目的探讨血清癌抗原199（CA199）、癌抗原125（CA125）、癌抗原153（CA153）和癌胚抗原（CEA）检测在对不同类型恶性肿瘤的诊断价值。方法采用全自动化学发光免疫分析法,检测62例不同类型肿瘤患者、14例非肺癌患者组及30例正常对照组血清CA199、CA125、CA153及CEA水平。结果胰腺癌患者组CA199、CEA水平显著高于对照组（P〈0．01、P〈0．05）,CA199的阳性率达100％;胃癌患者组CA199、CA125、CA153、CEA水平显著高于对照组（P〈0．01或〈0．05）：乳腺癌组CA153、CA125、CA199水平均明显高于对照组（P〈0．01或〈0．05）;卵巢癌患者组CA125,CA153水平显著高于对照组（P〈0．01或P〈0．05）;肺癌患者组CA199,CA125及CEA水平明显高于非肺癌对照组及正常对照组（P均〈0．01）。CA199、CA125及CEA联检特异性92．9％、敏感性79．3％。结论CA199测定对胰腺癌的诊断提供可靠依据。CA199、CA125及CEA联合检测对肺癌的诊断有重要意义。CA199、CA125、CA153及CEA4项指标联检对胃癌和乳腺癌的诊断有一定价值。CA125、CA153对卵巢癌的诊断有一定价值。     

乳腺癌手术前后血清CA153、CA125、CEA检测的临床意义

目的：探讨乳腺癌患者手术前后血清CA153、CA125和CEA水平的变化。方法：应用化学发光免疫分析法（CLIA）检测168例乳腺癌（Ⅰ＋Ⅱ期125例,Ⅲ＋Ⅳ期43例）患者血清CA153、CA125和CEA含量,并与132例非肿瘤患者作比较。结果：乳腺癌患者手术治疗前血清CA153、CA125和CEA含量非常显著地高于非肿瘤患者组（P〈0.01）;三者联合检测较单一检测阳性率明显增高（P〈0.01）。Ⅰ＋Ⅱ期患者手术后3个月CA153、CA125和CEA水平下降（P〈0.05）,与非肿瘤患者组比较无显著性差异（P〉0.05）;Ⅲ＋Ⅳ期患者手术后3个月CA153、CA125和CEA水平明显下降（P〈0.05）,但仍高于非肿瘤患者组（P〈0.05）。结论：检测乳腺癌患者血清CA153、CA125和CEA含量对临床诊断和预后观察具有重要的临床价值。     

肿瘤标志物CA153、CA125、CEA联合检测在乳腺癌中的临床应用

目的探讨肿瘤标志物CA153、CA120和CEA联合检测在乳腺癌中的临床应用价值。方法应用化学发光法测定20例健康对照者、20例乳房良性肿瘤、40例乳腺癌患者,及20例乳腺癌患者手术前后血清中CA153、CA125和CEA含量。结果乳腺癌患者血清中CA153、CA125、CEA的检测结果较其他两组的检测结果显著升高(P<0.01),其中,乳腺癌患者手术前血清CA153、CA125和CEA的水平明显高于手术后的水平(P<0.01)。联合检测的敏感性和特异性均明显高于单项指标的灵敏度和特异度。结论检测CA153、CA125和CEA对乳腺癌的诊断和治疗有使用价值。     

血清肿瘤标志物CA125、CA153、CEA水平检测在卵巢恶性肿瘤中的诊断价值

目的探讨血清肿瘤标志物癌抗原125（cancer antigen 125,CA125）、癌抗原153（cancer antigen 153,CA153）、癌胚托原（Carcinoembryonic antigen。CEA）单独或联合检测对卵巢癌的诊断价值。方法应用电化学发光技术测定经病理确诊的如矍癌患者152例、盆腔良性疾病患者68例及健康对照者80例血清肿瘤标志物CA125、CA153、CEA的含量水平,并计算各项目的阳性率、灵敏性、特异性、准确性等诊断性能指标。结果卵巢癌组3项肿瘤标志物水平显著高于卵巢良性疾病组及健康对照组（P〈0．01）;Ⅲ、Ⅳ期卵巢癌患者各指标阳性率高于Ⅰ、Ⅱ期患者（P〈0．05或P〈0．01）;上皮性癌患者各项指标阳性率高于非上皮性患者（P〈0．01）;判断卵巢肿瘤的良、恶性,单项指标以CA125的诊断性能最好;CA125、CA153、CEA联合检测可提高卵巢癌诊断的灵敏性和准确性（P〈0．01）。结论CA125、CA153、CEA单项检测对上皮性卵巢癌均有一定的诊断价值,其中以CA125诊断性能最高。且3项联检优于单项检测。     

检测CA125、CA153和CA72—4对卵巢癌诊断及疗效观察的临床价值

目的观察癌抗原125（CA125）、癌抗原153（CA153）、癌抗原72—4（CA72—4）对卵巢癌的诊断及疗效观察的价值。方法采用电发光法检测32例卵巢癌和21例妇科良性疾病患者血清中CA125、CA153和CA72—4水平。结果卵巢癌患者血清中CA125、CA153和CA72—4含量高于良性对照组,联合检测CA125和CA72—4特异性、敏感性优于单独检测及其它组合。卵巢癌患者治疗后CA125、CA153和CA72—4降低（P〈0．05～0．01）。结论联合检测CA125和CA72—4对卵巢癌的诊断有重要的临床价值,弥补了单独检测CA125的不足。     

血清CEA、CA125及CA153联合检测对肺癌诊断临床价值的探讨

目的探讨血清癌胚抗原（CEA）、糖类抗原125（CA125）及糖类抗原153（CA153）联合检测在肺癌诊断中的价值。方法收集278例肺癌患者血清,CEA、CA125、CA153测定采用美国ABBOTYAxsymx型电化学发光仪。结果肿瘤标志物CEA、CAt25、CA153CEA检测阳性率分别为41．0％、22．7％和13．3％。三项标志物联合检查至少有1项标志1次阳性的百分率为54．7％。3种肿瘤标志物在不同类型肺癌中的检测结果差异无显著性（P〉0．05）。结论CEA、CA125、CA153三项标志在NSCLC患者中有较高的阳性率,三项标志联合检测的阳性率高于任一标志单独检测的阳性率,联合检测有助于提高肺癌诊断的敏感性和准确性。     

血清CA125等4种肿瘤标志物联合检测对胸腔积液鉴别诊断的意义

目的：探讨肿瘤标志物联合检测在良、恶性胸腔积液鉴别诊断中鲫临床意义。方法：采集有胸腔积液患者的血清样本80例，其中恶性胸腔积液患者48例，良性胸腔积液患者32例，用多肿瘤标志物蛋白芯片检测系统检测血清CA125、CA153、CA99和CEA的含量。结果：恶性胸腔积液组血清CA125、CA153、CA199和CEA的水平明显高于良性胸腔积液组（P〈0．02）；联合检测可提高恶性胸腔积液诊断率。结论：肿瘤标志物CA125、CA153、CA199和CEA的联合检测，对胸腔积液的鉴别诊断有较好的临床价值。     

CA125、CA199和 CEA 联合检测在卵巢癌诊断中的临床意义

目的：探讨糖类抗原125（CA125）、糖类抗原199（CA199）和癌胚抗原（CEA）联合检测在卵巢癌诊断中的临床意义。方法选择我院收治的卵巢癌患者80例为研究组,卵巢良性疾病患者80例为对照 A 组,来院检查的健康者80例为对照 B 组,采用化学发光法对3组血清中 CA125、CA199和 CEA 含量进行测定。比较3种肿瘤标志物联合检测与单项检测 CA125的诊断意义。结果研究组3种肿瘤标志物水平及阳性率均显著高于对照组,且有显著性差异（P ＜0．05）。两对照组比较无显著性差异（P ＞0．05）。研究组单项检测及联合检测卵巢癌的阳性率均显著高于两对照组（P ＜0．05）。研究组联合检测阳性率为88．75％,明显高于单项检测的73．75％、43．75％和21．25％（P ＜0．05）。CA125、CA199和 CEA 单项检测比较,CA125的敏感性、特异性最佳。CA125的敏感性为73．75％,特异性为90．00％,阳性预测值为78．67％,阴性预测值为87．27％。除特异性外,联合检测的敏感性为88．75％、阳性预测值为79．78％、阴性预测值为94．04％,均较单项检测得以提高,且各指标更加趋于平衡。另外,联合检测对卵巢癌Ⅰ期、Ⅱ期的诊断有效率明显高于单项检测,且有显著性差异（P ＜0．05）。结论CA125、CA199和 CEA 3种肿瘤标志物联合检测能够早期有效地实现对卵巢癌的检测,对于卵巢癌病情的判断、治疗和转归有着重要的意义。     

血清CEA、CA199、CA125、CA153、AFP联合检测对胃癌的诊断价值

目的 探讨血清癌胚抗原（ CEA） 、糖链抗原199（ CA199） 、糖链抗原125（CA125）、糖链抗原153（CA153）、甲胎蛋白（AFP）单检和联检在胃癌中的诊断价值.方法采用化学发光免疫分析法检测50 例胃癌患者和65 例正常对照组的血清CEA、CA199、CA125、CA153、AFP的含量,分析五种肿瘤标志物单个检测和联合检测的敏感度、特异度.结果 胃癌患者的血清CEA、CA199、CA125的含量明显高于正常对照组（P＜0.05）;采用单项肿瘤标志物诊断胃癌时,灵敏度最高的为CEA和CA199,特异度最高的为CA153,ROC曲线下面积最大的为CEA;采用不同肿瘤标志物的组合诊断胃癌时,灵敏度和特异度均较好的为CEA、CA199与CA125组成的组合.联合检测和单独检测相比,敏感度显著提高,特异度有所下降.结论 联合检测可提高胃癌诊断的敏感度,为早期诊断及早期治疗提供有力的依据.     

合理补钙

钙是人体内含量最多的元素,约有1200 g,也是最容易缺乏的元素之一,其中99%形成骨骼,1%存在于血液和软组织.成人每日约有700 mg的钙进行更新.钙的吸收部位在小肠,主要在十二指肠,钙的吸收主要在活性V<,D3>的调节下进行.人体钙的90%的骨量在20岁以前积聚.35岁以后钙质逐渐流失,女性到绝经前钙流失的更快.因此,人的一生中,不仅要摄取足够的钙,以保证生命运动的需要,而且要保证钙的吸收,防止钙的流失.     

Comparative interactions of organic Ca++ channel antagonists with myocardial Ca++ and K+ channels

Dose-dependent inhibition by three organic calcium channel antagonists, D-600, nisoldipine and diltiazem, of the inward calcium current (iCa) and the delayed, outward potassium current (iK) in single frog atrial cells was examined using a voltage clamp technique. At holding potentials of -60 mV, low concentrations of these antagonists produced considerable inhibition of iCa without significant alterations in iK, suggesting that iK in single frog atrial cells is not a calcium-activated K+ conductance. Higher concentrations of each of these antagonists, however, inhibited iK. The estimated Kd values for inhibition of iCa and iK, respectively, were 3.7 X 10(-7) M and 8.2 X 10(-4) M for D-600, 1.6 X 10(-8) M and 1.6 X 10(-5) M for nisoldipine and 4.4 X 10(-6) M and 3.3 X 10(-4) M for diltiazem. Under these experimental conditions, D-600 and nisoldipine interact more selectively with myocardial Ca++ channels than K+ channels compared to diltiazem, which is less selective. In addition, the inhibition of iK by each of these antagonists was found to exhibit an apparent voltage dependence; block was enhanced at more negative membrane potentials and relieved at more positive membrane potentials. This voltage-dependent block of iK is, therefore, opposite to the voltage-dependent inhibition of iCa produced by these compounds, where block of iCa is accentuated at positive membrane potentials.     

Effects of 2-nicotinamidoethyl nitrate on agonist-sensitive Ca++ release and Ca++ entry in rabbit aorta

The effects of 2-nicotinamidoethyl nitrate (SG-75) on norepinephrine (NE)- and KCI-induced responses in rabbit aorta were quantitated, correlated with 45Ca studies and compared with the effects of nifedipine (NIF) on similar parameters. NE- and KCI-induced dose-response relationships were differentially depressed by SG-75 (NE much greater than KCI) and NIF (KCI much greater than NE). Responses to KCI were relatively insensitive to prior SG-75, yet moderately relaxed by subsequent SG-75. Conversely, NIF markedly inhibited and completely relaxed similar responses. Responses to NE were relaxed and inhibited with SG-75, but unaffected by NIF. Responses to NE in La or O-Ca++ + ethylene glycol bis(beta-aminoethyl ether)N,N'-tetraacetic acid plus D600 (with and without KCI) solutions were phasic, reduced by SG-75 and insensitive to NIF. NE-dependent, Ca++-induced responses in a O-Ca++ + ethylene glycol bis(beta-aminoethyl ether)N,N'-tetraacetic acid plus D600 solution (with and without KCI) were attenuated by SG-75. Equilibrated (60 min) La -resistant (residual), high apparent affinity Ca++ binding was increased 26% with SG-75 and decreased 34% with NIF, yet neither altered the rate of exchange (10 min). Rate of exchange at low apparent affinity, residual sites was increased 21% by SG-75 without altering equilibrated values, whereas NIF reduced equilibrated values 11%, without affecting rate. NE reduced, SG-75 + NE augmented and NIF + NE decreased, in an additive fashion, high apparent affinity, residual bound Ca++. Residual Ca++ binding at low apparent affinity sites was increased with 160 mM substituted KCI (380%). This increase was only partially inhibited with SG-75, and eliminated by NIF. Net Ca++ efflux was persistently slowed by SG-75 and unaltered by NIF. The primary effects of SG-75 appear to be depression of Ca++ release and inhibition of receptor-operated (potential-independent) Ca++ entry, with limited attenuation of voltage-dependent Ca++ entry. NIF primarily inhibits voltage-dependent Ca++ entry.     

Block of 45Ca uptake into synaptosomes by methylmercury: Ca++- and Na+-dependence

Block of Ca++ influx into isolated nerve terminals by the neurotoxicant methylmercury (MeHg) was studied for its dependence on extracellular Ca++ and Na+. Depolarization-independent entry of 45Ca++ was determined in rat forebrain synaptosomes incubated in 5 mM K+ solution. 45Ca++ uptake was similarly measured after 1 ("fast" phase) or 10 sec ("total") of elevated K+ (41.25 mM)-induced depolarization or after 10 sec of elevated K+-induced depolarization after synaptosomes had been predepolarized for 10 sec in Ca++- and MeHg-free solutions ("slow" phase). In 5 mM K+ solutions, MeHg concentrations of 125 microM and greater significantly reduced synaptosomal 45Ca++ uptake measured during 1 or 10 sec of incubation. In K+-depolarized synaptosomes, the estimated IC50 for block of total, fast and slow 45Ca++ uptake by MeHg is 75 microM; 250 microM MeHg reduced uptake by approximately 90%. The reversibility of block by extracellular Ca++ was tested by increasing the extracellular Ca++ concentration from 0.01 to 1.15 mM. When compared to control, 50 microM MeHg reduced total uptake of 45Ca++ by greater than or equal to 70% and reduced fast uptake by 20 to 60% at all concentrations of extracellular Ca++ tested. At Ca++ concentrations of 0.01 to 0.15 mM, MeHg (50 microM) reduced slow uptake by 75 to 90%, but did not affect slow uptake at higher Ca++ concentrations (greater than or equal to 0.30 mM). When the dependence of block of 45Ca++ uptake on extracellular Na+ was tested, equivalent levels of inhibition were caused by MeHg (25 microM) for fast uptake by synaptosomes in Na+-containing and Na+-free solutions.(ABSTRACT TRUNCATED AT 250 WORDS)     

Ca2+ extrusion across plasma membrane and Ca2+ uptake by intracellular stores.

The aim of this review is to summarize the various systems that remove Ca2+ from the cytoplasm. We will initially focus on the Ca2+ pump and the Na(+)-Ca2+ exchanger of the plasma membrane. We will review the functional regulation of these systems and the recent progress obtained with molecular-biology techniques, which pointed to the existence of different isoforms of the Ca2+ pump. The Ca2+ pumps of the sarco(endo)plasmic reticulum will be discussed next, by summarizing the discoveries obtained with molecular-biology techniques, and by reviewing the physiological regulation of these proteins. We will finally briefly review the mitochondrial Ca(2+)-uptake mechanism.