用免疫组化法对辐射致细胞凋亡与癌相关基因的研究

用免疫组化法对辐射致细胞凋亡与癌相关基因的研究［日］／长谷川正俊…∥日本医社会．一１９９５，５５（１１）．一７７９～７８０放射线引起的细胞凋亡在淋巴细胞、肠粘膜腺窝、高敏感的肿瘤等出现率较高。最近又有报道癌基因、癌抑制基因与细胞凋亡有关，文章就照射效...     

~(60)/钴γ线800拉德全身照射后大鼠小肠内分泌细胞的变化

本文观察到60/钴γ线800拉德全身照射后大鼠小肠亲银细胞和嗜银细胞同其它上皮细胞具有相似的损伤和修复过程。其中,十二指肠亲银细胞和嗜银细胞的数目,照后第2～3天比对照组显著减少(t>0.01),照后第5天显著增加(t>0.01)。肠腺的内分泌细胞损失较绒毛的少,恢复较绒毛的快。空、迴肠的变化和十二指肠相平行,但不如十二指肠明显,提示十二指肠内分泌细胞对辐射比空、迴肠更为敏感。     

X线头部照射对利血平处理雄性大鼠神经内分泌的影响

本研究试图观察10 GyX线头部照射后48小时对利血平处理雄性大鼠神经内分泌功能的影响。实验设正常对照、利血平处理和利血平处理加照射三组。结果证实,利血平处理组(动物每隔12小时注射一次利血平,0.5mg/kg BW,共注射6次)与正常对照组比较,神经内分泌功能发生明显改变;而利血平处理加照射组与利盥平处理组比较,血清LH、FSH、TSH、GH、T_3、T_4和睾丸酮水平只趋于降低,血清PRL和皮质酮(P<0.05)有不同程度增高,但这些结果尚无正常大鼠经10 GyX线头部照射后变化明显。提示,用利血平处理雄性大鼠神经内分泌系统功能发生复杂的改变,不能出现正常大鼠头部照射后48小时下丘脑—垂体—靶腺系统功能变化。     

X线头部照射对大鼠脾细胞ConA刺激反应及IL—2活性的影响

Wistar大鼠头部受10GyX线照射后48小时,脾细胞对ConA刺激反应明显增强。脾细胞浓度为5×10~6个/ml时,头部照射组与全身屏蔽照射组的反应比值平均为3.20(P<0.01),反应增强持续到照后5天(比值为3.09,P<0.05);脾细胞浓度为2.5×10~6个/ml时,反应比值为1.72(P<0.05),照后5天增强不显著。上述反应增强伴有脾重下降和有核细胞数减少。照后9天,反应达对照水平。头部10Gy照射后5天,脾细胞体外培养24小时的IL-2产量减少。照后2及9天变化不显著。实验结果说明,头部X线照射对机体免疫功能可产生明显影响。讨论了神经和内分泌系统在上述变化发生机理中的可能意义。     

萎缩小肠粘膜上皮细胞凋亡及增殖细胞核抗原表达变化的研究

目的：探讨小肠粘膜萎缩的发生机制。材料和方法;采用原位末端标记和免疫组化的方法,对正常和萎缩肠粘膜上皮细胞凋亡的发生,分布及增殖细胞核抗原（ＰＣＮＡ０的表达进行对比研究。结果：调亡细胞主要位于肠绒毛的顶部,萎缩小肠粘膜上皮细胞凋亡的发生率明显高于正常小肠（Ｐ〈０．０５）;而ＰＣＮＡ阳性表达细胞主要位于腺隐窝区,萎缩小肠粘膜上皮细胞ＰＣＮＡ的阳性计数较正常小肠显著降低。     

一种新的结直肠癌癌前病变——畸形腺窝灶

目前认为畸形腺窝灶 (ａｂｅｒｒａｎｔｃｒｙｐｔｆｏｃｉ,ＡＣＦ)是结直肠癌发生过程中可在光镜下观察到的最小最早期的大肠黏膜病变。虽然ＡＣＦ的真正性质还隐藏在诸多复杂有时甚至相互矛盾的研究结果中 ,但ＡＣＦ是最早的结直肠癌癌前病变的假说正被多数学者接受。传统的“腺瘤—腺癌顺序”途径可能扩展为“正常黏膜—ＡＣＦ—腺瘤—腺癌顺序”途径。对于ＡＣＦ的具体研究国内尚无相关报道 ,笔者就此作一综述。1　ＡＣＦ的发现史及一种新假说的提出Ｂｉｒｄ〔1〕在 1987年首次报道 ,在接受结肠致癌剂处理的鼠模型 (Ｃ5 7ＢＬ/ 6Ｊ或Ｃ…     

肠上皮化生的类型及其与胃癌发生的关系

肠上皮化生(简称肠化生),是一种后天性病变,常出现于胃的各种良性及恶性病,尤多见于慢性胃炎、胃溃疡及胃癌。近廿年来,各国学者应用组织化学、免疫组织化学、电镜、同位素自显影等方法,对肠化生进行了深入研究。本文主要探讨肠化生的类型及其与胃癌发生的关系。一、肠化生的来源早期的肠化生见于粘膜浅层。化生细胞来自腺颈部的未分化细胞。腺颈部是胃粘膜各型上皮的起源部,在生理性再生、修复以及各种粘膜病的增生中,新生的上皮细胞均来源于该部。在胚胎早期,内胚层发育成原始消化管,并进一步分化为消化     

十二指肠胃型上皮化生与幽门螺杆菌感染

对33例十二指肠溃疡患者手术标本的球部进行回顾性形态学观察,发现93.94%有胃型上皮化生。其中90.32%有幽门螺杆菌(HP)感染,67.74%伴活动性炎症,进一步证实胃型上皮化生、HP感染和十二指肠溃疡的密切关系。电镜观察18例十二指肠溃疡患者的活检球部粘膜,将胃上皮化生分为完全性和不完全性两类,后者为不成熟的粘液细胞,常保留肠吸收细胞的某些特征。化生细胞中的粘液与十二指肠腺内的粘液不同,显然化生细胞来源于腺窝内干细胞。根据HP寄居部位及其引起的细胞损害,表明其侵袭力及毒力不强。胃粘液在HP感染的建立和粘膜屏障方面具有双重作用,粘液数量和质量变化可能是HP致病过程中重要因素。     

在淋巴道转移过程中癌细胞在淋巴结内的命运及淋巴结的改变

以艾氏腹水癌细胞接种到小鼠右后肢掌内侧皮内,纪起腘窝淋巴结转移为模型,观察瘤细胞转移到淋巴结后的命运及淋巴结本身的变化。实验共四十天,在不同时间取其引流淋巴结往光学显微镜下观察。发现接种1小时后,瘤细胞可沿淋巴管移至腘窝淋巴结;5小时后瘤细胞有核分裂相,并可达第二站引流淋巴结,即髂动脉旁淋巴结;24小时后有明显的转移灶形成。瘤细胞进入淋巴结后由边缘窦到达中间窦,后达髓窦。三天后淋巴结出现明显的反应性增生,如毛细血管后小静脉周围出现许多运动型淋巴细胞、窦组织细胞增生和生发中心增大等。同时瘤细胞也开始出现变性及坏死的改变。电子显微镜下观察,发现淋巴结内的瘤细胞周围有许多淋巴细胞与之紧贴在一起,同时这些淋巴细胞胞浆中的线粒体及高尔基器均向细胞方向集结,并有向瘤细胞释放某种物质的现象。实验结果提示:加强和提高淋巴结防御肿瘤转移的能力,可能是抵抗肿瘤转移的重要途径之一。     

胎儿胃肠道胃泌素细胞与生长抑素细胞的免疫组织化学研究

本文用PAP免疫组织比学法和间接免疫荧光组织化学法,对60例8～38周胎儿胃肠粘膜中胃泌素细胞(G细胞)和生长抑素细胞(D细胞)的发生进行了研究。这两种细胞最早出现于8～9周胎儿十二指肠上皮中,但在固有膜及肌层未观察到。12周后,D细胞出现在胎儿胃肠全长粘膜,G细胞则只见于胃窦及小肠粘膜。本文还对各时期胎儿胃肠粘膜中D细胞和G细胞的分布、数量,以及二者比例变化等进行了观察。胃窦中G细胞与D细胞一样,基底部伸出突起,可能具有旁分泌功能。除胃底腺外,其余部位的D细胞和G细胞多为开放型细胞。本文对这两种细胞在胎儿胃肠发育中的可能功能进行了讨论,并与成人胃窦和十二指肠上部粘膜中G、D细胞的比例进行了对比观察。     

肠肌成纤维细胞与IBD相关肠纤维化

 肠纤维化是炎症性肠病(inflammatory bowel disease, IBD)的并发症,肠肌成纤维细胞是肠纤维化的关键细胞。肠肌成纤维细胞及其与炎症细胞的相互作用在IBD相关肠纤维化发生中起重要作用。     

Gastric and intestinal mixed and solely intestinal types of intestinal metaplasia in the human stomach

To generate a novel understanding of Intestinal metaplasia (IM) on the basis of cellular differentiation status, a total of 132 gastric surgical specimens were studied using gastric and small intestinal cell markers by much histochemical and Immunohistochemical techniques. The cases were divided into two types: (i) gastric and intestinal (GI) mixed type; and (ii) solely intestinal (I) type, with the reference to the presence of gastric and/or intestinal cell markers. The GI mixed type was subdivided into six subtypes: (i) a subtype consisting of surface mucous (Su), pyloric gland (Py), Intestinal absorptive (Ab), and goblet (Go) cells, but lacking Paneth (Pa) cells, GI(Pa-); (ii) a GI(Pa-) subtype without Py cells, GI(Py-, Pa-); (iii) a GI(Pa-) subtype without Su cells, GI(Su-, Pa-); (iv) a GI(Su-, Pa-) subtype with Pa cells, GI(Su-, Pa+); (v) a Gi(Pa-) subtype with Pa cells, GI(Pa+); and (vi) a GI(Pa+) subtype without Py cells, GI(–, Pa+).The I type was subdivided Into: (I) a subtype consisting of cells with Ab and Go cells, I(Pa-); and (ii) a I(Pa-) subtype with Paneth cells, I(Pa+). The GI mixed subtypes, except for the GI(Py-, Pa-) and GI(Py-, Pa+), were characterized by Intestinalized gastric plts connected with underlying pyloric glands. Immunohistochemical staining of proliferating cell nuclear antigen (PCNA) revealed a common prolifemtive cell zone between the two. The GI mixed type, especially the GI(Pa-) subtype, predominated in the pyloric mucose, while the I type was most frequent In the fundle region, suggesting that the pathogenesis of IM differs between these two locations. The results of the study confirm that IM is an abnormal and unstable differentiation status between the stomach and small Intestine.     

The physiology of intestinal oxygenation and the pathophysiology of intestinal ileus

Intestinal Ileus is Gut Shock caused by Bowel Hypoxia. The morbidity and mortality of Intestinal Ileus has puzzled more than two generations of investigators because they have overlooked the fact that the gas which collects in obstructed small intestine is mostly (90+%) Nitrogen. For some strange reason a gut full of nitrogen has not been looked on as comparable to a lung full of nitrogen, even though the lung and gut have a common embryological origin. My proposal is that intestinal epithelium lining a nitrogen filled lumen becomes as oxygen starved as alveolar lining in a similar circumstance. Bowel hypoxia may be brought about either by failure of the intestine to "breathe out", having breathed in due to mechanical block, or gut paralysis, from any cause, of which one may be failure of blood borne oxygen transport to the bowel, Individually, or together, these may reduce or stop the flow of air and/or aerated intestinal contents along the lumen. Local (bowel) or general underperfusion +/- hypovolaemia +/- anaemia may be a particular cause of paresis or paralysis (aperistalsis) of intestinal muscle. The non-contracting gut then fails to transport the luminal current of fluid and air (oxygen), and adds lumenal to blood-borne oxygen deficiency. The intestinal mucosa utilises oxygen from the current of air churned along the bowel by normal peristalsis to mix with and dissolve in the luminal contents. Should this current be obstructed or the propulsive churning activity cease, oxygen will be "used up", the residual gas become almost entirely nitrogen, and the mucosa must necessarily become oxygen starved and suffocated. Hypoxic mucosa lives in a dangerous environment, at risk of autodigestion by self-produced proteolytic or other enzymes secreted into the lumen by exocrine glands, and it may rapidly become necrotic and gangrenous. Different presentations of Ileus are different degrees of the same Gut Shock due to different levels and durations of tissue hypoxia brought about by different mechanisms with that final common path, complicated by different degrees of autodigestive mucosal destruction, bowel wall oedema, and fluid exudation into the lumen comparable to that through BURNED skin. This idea is new only in so far as it has been put together in this way. Parts have been anticipated by other writers. No new ways of managing ileus are proposed, but it is suggested that existing empirical methods be rationalised and applied more widely and logically.     

Importance of the intestinal inflammatory reaction in salmonella-mediated intestinal secretion.

The ability of Salmonella typhimurium to invade the intestinal epithelium is essential to the pathogenesis of salmonella-induced intestinal secretion. This invasion is accompanied by an intense acute inflammatory reaction. The present study tests the hypothesis that the acute inflammatory reaction may have a role in the pathogenesis of salmonella-induced secretion. Two groups of rabbits infected with S. typhimurium were studied: normal animals and animals pretreated with nitrogen mustard. Nitrogen mustard depletes the polymorphonuclear leukocyte pool and thereby prevents the formation of an acute inflammatory reaction. In vivo ligated ileal loops were constructed and infected 72 h after nitrogen mustard administration when polymorphonuclear leukocytes were undetectable. Nitrogen mustard treatment markedly inhibited salmonella-induced secretion. Ileal histology in normal animals infected with S. typhimurium revealed an intense acute inflammatory reaction, while in animals pretreated with nitrogen mustard only a rare polymorphonuclear leukocyte was seen. The antisecretory effect of nitrogen mustard was not merely a nonspecific effect since nitrogen mustard treatment did not inhibit cholera toxin-induced secretion and did not alter either ileal morphology nor the activities of various intestinal enzymes in normal animals. Nitrogen mustard also did not alter the virulence of the inoculated S. typhimurium. These data suggest that the mucosal inflammatory reaction induced by salmonella invasion may be important to the pathogenesis of the salmonella secretory process. The mechanism by which the inflammatory reaction stimulates secretion is not known.     

肠血管活性多肽或生长抑素对大鼠肠淋巴细胞在肠淋巴组织分布的影响

目的：观察肠血管活性多肽（VIP）或生长抑素（SST）对大鼠肠淋巴细胞归巢至肠相关淋巴组织（GALT）的影响。方法：从肠系膜淋巴管插管引流淋巴液，淋巴细胞经VIP和SST体外孵育后，用^51Cr标记，将^51Cr-肠淋巴细胞朋股静脉回输入大鼠体内。取出各组织、器官，用γ计数器检测其放射性活度。结果：生理状况下，约10％^51Cr-肠淋巴细胞在短期内归巢至GALT。经VIP或SST孵育的^51Cr-肠淋巴细胞回输入大鼠体内后，在肠系膜淋巴结（1．85％，1．60％）用Peyer结（1.83%,1.56%)分布的百分比显著低于对照组（3．83％，3．85％），P＜0．05）。2种多肽对^51Cr-肠淋巴细胞在小肠弥散淋巴组织的分布无明显影响。结论：VIP或SST对大鼠肠淋巴细胞归巢至Peyer结和肠系膜淋巴结有一定的抑制作用。