Changes of Intestinal Caicitonin Gene-related Peptide in Acute Intestinal Radiation Sickness in Rats

The characteristic distribution of calcitonin gone-related peptide(CGRP)inthe small intestine of rats and its changes in acute intestinal radiation sickness(AIRS)were studied with immunocytochemistry(whole mount stretch preparations of the smallintestine and cryostat sections)and radio-immunoassay.It was found that in all the lay-ers of the intestinal walls,there were large amounts of CGRP immunoreactive(CGRP-I)nerve fibers which existed in especiaUy high density in the myenteric,submucosal andmucosal plexuses.There was also a rather high density of the nerves around the smallvessels of the small intestine and the intestinal crypts.Some CGRP-I neurons were seenin the myenteric and submucosal plexuses.In AIRS,the intestinal CGRP showed a dip-hasic change,in a lower level in the 24th h and a higher level in the 48th and 72nd h af-ter irradiation.The results indicate that CGRP may be related to the regulation of the motility,se-cretion,absorption,sensation,and regional blood flow of the gastrointestinal tract.Pro-bably,CGRP is released under the stress of AIRS and participates in the mechanism ofinjury through many ways especially through the influence on the regional blood flowand the increase of the permeability of blood vessels.     

536例大肠癌误诊误治分析

大肠癌误诊误治较为普通。从总结经验教训出发，本文对确诊前曾发生过误诊误治的５３６例大肠癌进行详尽的分析。本组病例５３６例，曾７１９次先后被误诊为３２种疾病，其中误诊为“痔”“痢疾”“肠炎”“肠梗阻”等最为常见，误诊为其它疾病也时有发生，严重的影响其预后。在误诊原因上，除病人自误外，与医生责任心不强，询问病史不细，本行或未认真行有关检查，特别是直肠指诊检查和结肠内窥镜检查是分不开的。文章就今后如何减少误诊，提高早期诊断率，提出了５点措施，强调了直肠指诊和结肠内窥镜检查的重要价值。     

人大肠癌细胞体外常温及温热环境中药物敏感性试验

用ＭＴＴ比色法对２０例大肠癌患者术后标本在常温及温热环境中进行体外药物敏感性试验，结果显示，某些药物在温热环境中，对癌细胞的杀伤作用有显著提高，此项试验为临床温热化疗法提供了理论依据。     

围术期维持活体部分移植小肠血供的措施

目的：探讨围术期维持移植小肠血液灌注的方法，方法：男，18岁，短肠综合征患者，全麻下接受其父亲供给末段回肠150cm，行活体部分小肠移植，围主期维持出入量平衡，中度等容血液稀释，选用扩血管药，防止血管痉挛，以及抗凝治疗，结果：术的31d脱离肠外营养，至今已术后34mo，未发生移植小肠明显缺血性改变。结论：采用上述方法匀是维持围术期移植小肠血供的重要措施。     

Interdigestive small bowel motility and duodenal bacterial overgrowth in experimental acute pancreatitis

The objective of this study is to investigate the effects of an acute necrotizing pancreatitis (ANP), without biliary obstruction, on the migrating motor complex (MMC), small bowel bacterial overgrowth (SBBO), bacterial translocation (BT) and infection of the pancreas simultaneously. Rats were divided into four groups: mild pancreatitis, control, ANP and sham operated control. Jejunal myoelectrodes were used to measure MMCs. Blood, peritoneal fluid, bile, and abdominal organs were harvested for microbial culturing 72 h after induction of pancreatitis. The splenic portion of the pancreas was taken for histology. During ANP the MMC cycle length was significantly increased from 14.1 +/- 0.2 to 22.4 +/- 1.9 min (P < 0.05). The duodenum of ANP rats was in contrast with the other groups characterized by Enterobacteriacae (> 3 log 10 CFU g-1 in seven of 12 rats, P < 0.05). A positive correlation (r = 0.78, P < 0.01) existed between duodenal Gram-negative and anaerobic flora and the MMC cycle. Correlation between MMC cycle length and BT to the pancreas was positive as well (r = 0.70, P < 0.01). A positive correlation (r = 0.85, P < 0.01) was found between the severity of pancreatitis and duodenal bacterial overgrowth. During ANP without biliary obstruction, the jejunal MMC is disturbed and consequently SBBO occurs. The correlation between the severity of pancreatitis, the disturbance of the MMC and SBBO suggests an important pathophysiological role of the proximal small bowel in the infection of pancreatic necrosis.     

青年人大肠癌误诊原因探讨

目的 探讨青年人大肠癌的误诊原因，以便早期诊断治疗。方法 回顾性分析62例青年人大肠癌的诊断及其治疗效果。结果 本组直肠癌36例中被误诊为结肠炎7例，痔疮并出血5例，痢疾3例，肛周脓肿并肛瘘2例；结肠癌26例中被误诊为阑尾周围脓肿3例，结肠炎2例，缺铁性贫血1例。误诊率37．1％。结论 青年人大肠癌早期临床症状不明显，恶性程度高，预后差,其治疗水平有赖于对这些特征的认识，力争早期诊断及治疗。     

A new monoclonal antibody which binds to the cytoplasm of large cell lymphomas.

We reported a new monoclonal antibody, designated FUB-1, reacting with normal and neoplastic large lymphoid cells. FUB-1 was produced using a Burkitt's lymphoma cell line (HBL-5) as an immunogen. Its immunoglobulin subtype was IgM. The determinant was not on the surface but in the cytoplasm. Western blotting analysis revealed that the molecular weight of the antigen was 52,000 dalton. In the normal lymphoid tissue, FUB-1 reacted with large lymphoid cells, but not with small or medium-sized lymphoid cells or plasma cells. In addition, the FUB-1 antigen was not found in resting cells in the peripheral blood (PB), but it was induced on mononuclear cells of PB by addition of PWM or PMA. In the B-cell lymphomas tested, FUB-1 reacted with small cleaved cell lymphomas (3/12), large cell lymphomas (7/10), Burkitt's lymphomas (4/4) and immunoblastic lymphomas (2/2), but not with small cell lymphomas (0/3) or intermediate lymphocytic lymphomas (0/8). These findings indicate that the FUB-1 antigen appears to be expressed on normal lymphoid cells during blastoid transformation and on neoplastic large lymphoid cells. FUB-1 also reacted with normal glandular epithelium and various adenocarcinomas. FUB-1 may be useful to investigate the mechanism of in vitro blastoid transformation or activation of lymphoid cells.     

THE PHARMACOLOGICAL ROLE OF P-GLYCOPROTEIN IN THE INTESTINAL EPITHELIUM

P-glycoprotein, a membrane-associated transport protein, has recently been recognised as an important element of the intestinal epithelium. This paper summarises thein vivodata on the pharmacological role of intestinal P-glycoprotein. These data show that P-glycoprotein contributes to the elimination of many drugs by mediating their direct secretion from the blood into the intestinal lumen. In addition, there is also evidence that this protein can limit oral drug absorption. Hence, inhibition of intestinal P-glycoprotein, e.g. by a reversal agent like cyclosporin A, may be a promising strategy for improving the oral bioavailability of P-glycoprotein substrate drugs. Indeed, several preclinical and clinical studies have shown that coadministration of drugs with a reversal agent can substantially increase oral drug absorption.     

Role of 4-1BB in Allograft Rejection Mediated by CD8+ T Cells

Blockade of traditional costimulatory molecules fails to inhibit rejection in many models where CD8+ T cells are sufficient to mediate rejection. This observation demonstrates that in many settings CD8+ T cells are not dependent upon CD28 or CD154 signals to mediate rejection. 4-1BB (CD137) has been shown to be an important regulatory molecule for CD8+ T cells in a variety of nontransplant models. Here we show that blocking the 4-1BB pathway significantly inhibited rejection of intestinal allografts by CD8+ but not CD4+ T cells. This effect was associated with significantly decreased expression of the genes encoding TNFalpha and secondary lymphoid chemokine (SLC) within the spleens of recipient mice. Disruption of the 4-1BB pathway also impaired the priming of alloantigen-specific CD8+ T cells and the accumulation of recipient dendritic cells within the spleen. These data directly demonstrate an important role for 4-1BB in allograft rejection; particularly rejection mediated by CD8+ T cells. Our data suggest that in addition to providing a direct costimulatory signal to T cells, the 4-1BB pathway may regulate other important steps in the immune response such as the migration of T cells and dendritic cells.     

Effect of L(+)-tartrate on some biochemical and enzymatic parameters in normal and glycollate treated rats

Some biochemical and enzymatic constituents were determined in the small intestinal tract tissues of normal and sodium glycollate treated adult male rats. Alterations were observed with respect to certain lipids and carbohydrate fractions in the glycollate fed rats. DNA content was also elevated in this group. The functions of the cell membrane is likely to be affected as reflected in the levels of transport ATPases and orthophospho-hydrolases. The activities of the two marker enzymes in the intestinal brush border, namely alkaline phosphatase and leucylnaphthylamidase were reduced in the glycollate administered group. Administration of L(+)-tartrate, which is a mild laxative and has a regulatory influence on oxalate metabolism, lowered the activities of Na+, K(+)- and Ca(2+)-ATPases. There was a distinct lowering in the level of acid phosphatase in the tartrate treated rats.