肺癌CDKN2基因产物表达的研究

目的观察ＣＤＫＮ２基因产物（Ｐ１６蛋白）在肺癌和癌旁正常组织的表达情况，了解该基因与肺癌的关系。方法采用ＳＰ免疫组织化学方法观察ＣＤＫＮ２基因产物在１３９例肺癌组织的表达情况，并与癌旁正常组织进行对比。结果Ｐ１６蛋白在良、恶性细胞的胞浆中均有表达，癌旁正常支气管粘膜上皮和浆液腺Ｐ１６蛋白的阳性率高于癌组织（Ｐ＜０．０１）。肺癌组织中Ｐ１６蛋白的总阳性率为６１．９％，腺癌的阳性率高于鳞癌和小细胞癌（Ｐ＜０．０１）。在鳞癌和腺癌Ｐ１６蛋白的阳性率随着分化程度的降低而下降，高分化和低分化腺癌之间Ｐ１６阳性率的差异有显著性（Ｐ＜０．０５）。结论Ｐ１６蛋白表达缺失与肺癌的发生有关，且随着分化程度的下降表达缺失增加。     

大肠癌及癌旁内分泌细胞的表达意义

目的探讨内分泌细胞（ＥＣ）在大肠癌及癌旁的表达意义．方法应用ＬＳＡＢ免疫组化法，对１１７例大肠癌及８５例癌旁粘膜中嗜铬蛋白Ａ（ＣＧＡ）及几种激素进行检测，１３例大肠癌行电镜观察．结果ＥＣ阳性大肠癌４６例（３９３％），检测到一种以上激素６９２％（２７／３９），癌旁粘膜ＥＣ数高于正常肠粘膜．电镜观察８例有含内分泌颗粒的癌性ＥＣ．在中低分化癌中ＥＣ（＋＋）的表达（２５５％）高于高分化癌（６９％）（χ２＝７５４，Ｐ＜００５），含有ＥＣ的大肠癌淋巴结转移的发生率（６８０％）高于不含ＥＣ者（４３７％）（χ２＝６２３，Ｐ＜００５），且预后不良；５ＨＴ，βＨＣＧ，Ｇｌｕ，Ｇａｓ阳性癌分化及预后较差（Ｐ＞００５）．结论含ＥＣ的大肠癌具有更恶性的生物学行为，可能与ＥＣ中某些激素，通过旁分泌等途径促进肿瘤的生长转移有关，癌旁ＥＣ增生与周围肿瘤生长有关．     

单克隆抗体SC3A在胃癌及癌前病变的表达意义

目的研究单克隆抗体ＳＣ３Ａ在胃癌及癌前病变的表达意义．方法应用免疫组化ＡＢＣ法及粘液组化染色检测１０１例胃良恶性病变组织中ＳＣ３Ａ的表达．结果胃癌７１例中ＳＣ３Ａ阳性５７例（８０３％），但与癌组织类型、分化程度、转移及术后生存率无明显关系．ＳＣ３Ａ阳性率在酸性粘液（＋）组胃癌明显高于酸性粘液（－）组（９０２％对２００％，Ｐ＜００１），硫酸粘液（＋）组胃癌明显高于硫酸粘液（－）组（９１３％对６００％，Ｐ＜００１）．而且癌旁肠化硫酸粘液阳性率明显较良性病变伴肠化高（８８９％对３５３％，Ｐ＜００１）；硫酸粘液（＋）组肠化ＳＣ３Ａ阳性率明显高于硫酸粘液（－）组（６０９％对３１３％，Ｐ＜００５）．结论单克隆抗体ＳＣ３Ａ的表达对胃癌诊断及组织发生探讨有一定意义．     

自由基在实验性胃癌及癌前病变发生中的作用

目的探讨自由基在胃癌及其癌前病变发生中的作用．方法将１００只Ｗｉｓｔａｒ大鼠分为２组，实验组（７０只），给予１００ｍｇ／Ｌ甲基硝基亚硝基胍（ＭＮＮＧ）水溶液自由饮用３０ｗｋ，对照组（３０只）饮用自来水．选５个时相点，动态观察ＭＮＮＧ诱发实验性胃癌及其癌前病变过程中大鼠体内丙二醛（ＭＤＡ）、脂质过氧化物（ＬＰＯ）、谷胱甘肽过氧化物酶（ＧＳＨＰＸ）及超氧化物歧化酶（ＳＯＤ）等的变化情况．结果在实验组，ＭＤＡ平均含量在５２ｗｋ非常显著地大于０ｗｋ（Ｐ＜００１），并显著地大于１６ｗｋ以前（Ｐ＜００５）．胃癌组织ＭＤＡ含量显著高于胃癌癌前病变组织（Ｐ＜００５）．癌组织ＬＰＯ的含量显著高于癌前病变组织（Ｐ＜００５）．实验组，总ＳＯＤ和ＣｕＺｎＳＯＤ活性在５２ｗｋ明显低于１６ｗｋ之前（分别为Ｐ＜００５和Ｐ＜００１）．癌组织ＣｕＺｎＳＯＤ含量非常显著地小于正常胃粘膜（Ｐ＜００１），亦明显低于胃粘膜异型增生和肠上皮化生（Ｐ＜００５）．在３０ｗｋ和５２ｗｋＧＳＨＰＸ活性显著低于１６ｗｋ以前．结论自由基在实验性胃癌及其癌前病变发生中具有一定作用，自由基清除剂可能对胃癌的综合防治具有积极意义     

基质金属蛋白酶-2 mRNA在胃癌中的表达

目的　探讨基质金属蛋白酶２（ＭＭＰ２） ｍＲＮＡ 及蛋白在胃癌中的表达。方法　用ＲＴＰＣＲ 法及免疫组化法分别检测２５ 例胃癌患者癌组织及癌旁２ｃｍ 与≥５ｃｍ 组织ＭＭＰ２ ｍＲＮＡ 及蛋白的表达。结果　胃癌组织ＭＭＰ２ ｍＲＮＡ 表达率（１７／２５） 高于两组癌旁组织，与癌旁≥５ｃｍ 组织表达率（９／２５）比较差异有显著性（Ｐ＜０ ．０５）；免疫组化显示胃癌组织ＭＭＰ２ 蛋白的表达率（１７／２５） 也高于两组癌旁组织，与癌旁≥５ｃｍ 组织表达率（８／２５） 比较差异有显著性（Ｐ＜ ０ ．０５） 。结果接近ＲＴＰＣＲ 法；胃癌组织ＭＭＰ２ ｍＲＮＡ 表达值显著高于两组癌旁组织（Ｐ均＜０ ．０１）；ＭＭＰ２ ｍＲＮＡ 及蛋白表达似与胃癌分化及临床分期有关。１９ 例进展期胃癌组织及癌旁２ｃｍ 组织，ＭＭＰ２ ｍＲＮＡ 表达值显著高于６ 例早期胃癌相应组织（Ｐ均＜ ０．０５） 。结论　ＭＭＰ２ 在胃癌侵袭及转移过程中可能发挥重要作用。     

胃肠肿瘤组织中纤溶酶原激活剂的测定及其价值

采用ＥＬＩＳＡ在胃肠肿瘤的手术切除组织和胃癌的胃镜活检组中检测纤溶酶原激活剂（ＰＡｓ）抗原，结果显示癌组织中ｕ－ＰＡ含量同于对应的正常组织（Ｐ＜０．０１），ｔ－ＰＡ含量在肿瘤与正常组织中相似；有淋巴结转移者的癌组织中ｕ－ＰＡ含量显著高于淋巴结转移者（Ｐ＜０．０５）；病灶较大的肿瘤组织中ｕ－ＰＡ含量与病灶小者相比差异有显著性（Ｐ＜０．０５）；分化差的癌组织中ｕ－ＰＡ含量亦高于分化好者。同一患者在活检     

胃癌患者血清可溶性白细胞介素—2受体初步研究

应用双抗体夹心ＥＬＩＳＡ法对３０例胃癌患者血清ＳＩＬ－２Ｒ水平进行测定，结果表明，胃癌患者血清ＳＩＬ－２Ｒ水平明显高于正常对照（Ｐ＜０．０１）及慢性良性胃病患者（Ｐ＜０．０５）；Ⅲ－Ⅳ期患者血清ＳＩＬ－２Ｒ水平显著高于Ｉ－ＩＩ期患者（Ｐ＜０．０５）；低度分化者较中度分化者ＳＩＬ－２Ｒ水平明显升高（Ｐ＜０．０１）；贲门癌患者ＳＩＬ－２Ｒ水平较胃窦（体）癌者高，但未达到统计学差别（Ｐ＞０．０５）；胃癌     

胃癌组织5q微卫星不稳定性与APC/MCC基因杂合性缺失的研究

目的探讨５ｑ微卫星不稳定性（ＭＳＩ）与ＡＰＣ／ＭＣＣ基因杂合缺失（ＬＯＨ）的关系。方法应用ＰＣＲ－ＳＳＬＰ及ＰＣＲ－ＲＦＬＰ技术分析５２例手术切除胃癌组织中ＭＳＩ及ＡＰＣ／ＭＭＣ基因ＬＯＨ。结果５ｑＭＳＩ检出率为３４．０％（１６／４７）,ＡＰＣ／ＭＣＣ基因ＬＯＨ率为３１．４％（１１／３５）。早期胃癌５ｑＭＳＩ阳性率为６６．７％（２／３）,ＡＰＣ／ＭＣＣＬＯＨ率为５０％（１／２）;进展期分别为３１．８（１４／４４）,３０．３％（１０／３３）。两组间无显著差别（Ｐ＞０．０５）。ＭＳＩ及杂合缺失与肿瘤大小、浸润深度、淋巴结转移及临床分期无关。粘液（印戒）细胞癌ＡＰＣ／ＭＣＣＬＯＨ率（５５．６％）显著高于高、中分化管状腺癌（Ｐ＜０．０５）。胃、肠两型胃癌５ｑＭＳＩ及ＡＰＣ／ＭＣＣＬＯＨ差异无显著性及５ｑＭＳＩ与ＡＰＣ／ＭＣＣＬＯＨ无相关性（Ｐ＞０．０５）。结论染色体５ｑＭＳＩ有ＡＰＣ／ＭＣＣ基因ＬＯＨ在两型胃癌的早期发生及发展中起一定作用。染色体５ｑ可能是胃癌的易感部位。     

血清癌胚抗原,糖链抗原及血清铁蛋白检测地大肠癌的诊断价值

用放射免疫法检测４１例大肠癌患者和２０例结肠炎患者血清ＣＥＡ、ＣＡ１９－９、ＳＦ含量。结果显示：大肠癌三项标记测定植均明显高于对照组（Ｐ〈０．０１）。三项指标中除ＣＥＡ在Ａ２期较高外，基本符合病理进行程序越深，肿瘤标记物检出率越高的标点。组织学分类中ＣＥＡ阳性率粘液腺癌〉乳头状腺癌，ＣＡ１９－９粘液腺癌〉管状腺癌〉乳头状腺癌，ＳＦ则管状腺癌明显〉乳头状腺癌（Ｐ〈０．０５）。三项标记物联合检测时其敏     

8种肿瘤相关抗原在活检胃粘膜病变组织中的表达

应用免疫组织化学方法观察了８种肿瘤相关抗原（ＭＧ７、ＭＧｄ１、ＭＣ３、ＣＥＡ、涎酸化糖蛋白、ＣＡ１９─９、ＰＳ─４和ＴＡＧ─７２）在１１０例胃癌、３２例异型增生，１７３例萎缩性胃炎和２０例大致正常胃粘膜活检组织中的表达，发现胃癌组８种肿瘤相关抗原染色的阳性率显著高于良性病变和正常对照组（Ｐ＜０．０１～０．００１）。异型增生组和萎缩性胃炎组８种肿瘤相关抗原阳性率均显著高于正常对照组（Ｐ＜０．０５～０．０１）。除ＭＣ３外，各抗原在胎儿胃或肠粘膜均有部分阳性。以上结果说明，检测胃粘膜组织中的上述８种抗原，对胃癌的诊断和高危人群的筛选可能有重要意义。     

IN AND OUT

No abstract available for this article.     

CORTICOTROPIN-LIKE PEPTIDES IN CENTRAL NERVES AND IN ENDOCRINE CELLS OF GUT AND PANCREAS

Extrapituitary corticotropin-like peptides have been found in central nerves and in gastrointestinal and pancreatic endocrine cells. Previous biological and immunological data strongly indicate that the immunoreactivity present in the central nerves represents corticotropin (A.C.T.H.) or a closely related peptide. In some areas of the brain, the distribution of A.C.T.H. nerves parallels that of nerves containing the endogenous opioid ligand, enkephalin. Since A.C.T.H. fragments bind to the opioid receptor the two neuronal peptides may interact. The antiserum used demonstrates the COOH-terminus of the A.C.T.H. molecule, which is devoid of adrenocortical stimulatory activity. A COOH-terminal A.C.T.H.-peptide, corticotropin-like intermediate peptide (C.L.I.P.), originally isolated from the pars intermedia, has been shown to stimulate release of pancreatic insulin. The presence of C.L.I.P.-like molecules in gut and pancreatic endocrine cells may indicate that C.L.I.P.'S insulin-releasing activity is physiologically important. Further, the occurrence of A.C.T.H.-related molecules in such cells may account for the ectopic A.C.T.H. syndrome associated with some tumours of gut and pancreas.     

CHANGES IN CORTICAL AND TRABECULAR BONE IN ALGODYSTROPHY

We studied the pattern of bone loss in the hand of 77 patientswith Colles' fracture using metacarpal morphometry, single photonabsorptiometry and a radiographic scoring system. Forty-fourpatients had post-traumatic algodystrophy and the remainderserved as controls. Both groups were immobilized in the samemanner and for the same period of time and both showed lossof bone during immobilization. The loss of bone 7 weeks afterfracture was significantly greater in algodystrophy than incontrols both at cortical (P<0.05) and at trabecular sites(P<0.05). Recovery of bone occurred in the control patientsby 19 weeks after fracture at cortical sites and by 31 weeksin trabecular bone. In contrast, the bone loss seen in patientswith algodystrophy persisted for the 6-month duration of thefollow-up, and up to 1 year in all nine patients studied forlonger. These findings indicate that post-traumatic algodystrophyis associated with regional skeletal losses greater than thosefollowing uncomplicated fracture and may result in irreversiblechanges in the structure and thus the strength of the bony architecture. KEY WORDS: Colles' fracture, Bone density, Photon absorptiometry, Metacarpal morphometry, Immobilization, Reflex sympathetic dystrophy     

SKIN COLLAGEN AND THICKNESS IN HYPERTHYROIDISM AND MYXOEDEMA

Skin thickness, collagen content and density have been measured in patients with thyrotoxicosis and myxoedema. In hyperthyroidism the skin was of normal thickness but the absolute collagen content and density of collagen were both increased as was the percentage collagen content. In myxoedema both absolute percentage collagen content and density remained normal but the skin thickness was significantly increased and this correlated well with the severity of hypothyroidism and response to treatment.     

青海省人与动物多房棘球绦虫的感染

本文报告 195 9～ 1998年青海高原人与动物多房棘球绦虫感染情况的研究结果。共手术治疗泡型包虫病人111例 ;男性 73例 ,女性 38例 ;其中肝泡球蚴病 10 0例 ,肺泡球蚴病 2例 ,脑泡球蚴病 7例 ,脾泡球蚴病 2例。年龄17～ 74岁 ,成年人最为常见。牧民和农民最多见 ,其他职业少见。普查 370 2人 ,B超诊断为肝泡球蚴病者 2 3人( 0 .6 2 % ) ,EM1 8血清学阳性者 30人 ( 0 .81% ) ,两种方法均符合者 13人 ( 0 .35 % )。调查中间宿主 7种 ,在家养动物牦牛肝脏和肺脏及藏绵羊肝脏发现泡球蚴感染 ,感染率分别为 4.0 9% ( 18/ 384)和 5 .36 % ( 31/ 5 78) ;野生动物黑唇鼠兔的肝脏和肺脏及灰尾兔的肺脏发现泡球蚴的感染 ,其感染率分别为 3.45 % ( 11/ 319)和 12 .5 0 % ( 1/ 8)。调查终宿主 5种 ,在藏犬和藏狐肠内均证实多房棘球绦虫感染 ,其感染率分别为 5 .0 8% ( 3/ 5 9)和 33.33% ( 4/ 12 )。提示青海高原存在多房棘球绦虫的藏犬、藏狐 /黑唇鼠兔、灰尾兔和藏犬、藏狐 /牦牛、藏绵羊两种类型的多房棘球绦虫生活史循环链     

中国地鼠糖尿病模型胰岛A,B细胞数量及分布改变

应用免疫组织化学及图像分析的方法,研究中国地鼠遗传性糖尿病模型胰岛A、B细胞,发现该糖尿病模型中胰岛的病变程度不一,A、B细胞的数量和分布均有改变,光镜见糖尿病鼠胰岛B细胞染色的平均光密度的分布范围大于对照54.4％,胰升血糖素阳性免疫反应物占胰岛面积百分比31.6％±13.2％,显著高于对照组（21.8％±7.5％）。     

INTERACTION OF CLONIDINE AND GHRH ON GH SECRETION IN VIVO AND IN VITRO

To investigate the mechanism by which clonidine stimulates GH-secretion in vivo and in vitro, we studied its interaction with GHRH. In vivo: eight or six normal male subjects were submitted to five protocols: (1) 150 micrograms clonidine orally followed by 50 micrograms GHRH 1-44 i.v. 2 h later, (2) 50 micrograms GHRH 1-44 i.v. followed by 150 micrograms clonidine orally 2 h later, (3) 150 micrograms clonidine orally followed by GHRH i.v. 30 min later, (4) 300 micrograms clonidine orally followed by 50 micrograms GHRH i.v. 3 h later and (5) 50 micrograms GHRH i.v. followed by 300 micrograms clonidine orally 90 min later. In vitro: Rat anterior pituitary cells were coincubated with clonidine (10(-11), 10(-9), 10(-7) and 10(-5) M) and GHRH (0.005, 0.05, 10 nM) for 4 h. Results: 150 micrograms clonidine alone does not stimulate GH-secretion. Furthermore, the GH-increase was not significantly different when GHRH bolus was given before, after or together with clonidine. When 300 micrograms clonidine was given before GHRH GH-levels were significantly higher (max 28.6 +/- 8.0 mU/l) at 90 min, compared to when clonidine was given after GHRH (max 7.8 +/- 3.6 mU/l). The GHRH bolus after clonidine led to a significantly lower GH-increase (max 31.6 +/- 17.0 mU/l) compared to the GHRH-induced GH-increase (max 47.2 +/- 13.0 mU/l) before clonidine. In vitro, clonidine had no stimulatory effect on GHRH-stimulated GH secretion. These findings are compatible with clonidine leading to stimulation of GH by inducing endogenous GHRH release.