胰弹力蛋白酶I和核糖核酸酶检测的临床价值

目的　探讨人胰弹力蛋白酶Ⅰ (Humanpancreaticelastase 1 ,HPE1 )放射免疫测定 (Radioimmunoassay ,RIA)和核糖核酸酶(Ribonuclease ,RNase)活性检测的临床价值。方法　参照Satake等建立的改良HPE1RIA和Thomas等的改良酸溶性产物法检测 82例正常成年人和 2 2 2例各类患者血清并分析结果。结果　 82例健康成人HPE1值为 2 3.8( 3.4ng L) ,RNase活性为 5 7.0 3( 1 2 .1 6 μ ml) ;急性胰腺炎和胰腺癌HPE1 值明显高于其他疾病 (P <0 .0 1 )。联合检测HPE1 、RNase活性可提高胰腺癌的检出率 ( 92 .47% )。结论　HPE1 RIA对急性胰腺炎有诊断价值 ,联合检测HPE1 、RNase活性检测对胰腺癌诊断有一定的临床价值     

腺病毒介导的CD基因在人胰腺癌细胞中的靶向性表达

【目的】探讨腺病毒介导的大肠杆菌胞嘧啶脱氨酶 (E .coliCD)基因在胰腺癌细胞中靶向性表达的可能性及其作用。【方法】将含癌胚抗原 (carcinoembryonicantigenCEA)启动子的重组腺病毒感染人胰腺癌SW1990细胞 (CEA )、Capan 2细胞 (CEA-)和人宫颈癌Hela细胞 ,观察CD基因在 3种细胞中的表达及细胞对 5 FC的敏感性差异。【结果】腺病毒介导CD基因仅在SW1990细胞中呈专一性表达 ,转导CD基因的SW1990细胞对 5 FC的敏感性明显提高。【结论】含CEA启动子的CD基因疗法可能是胰腺癌靶向性基因治疗的可行途径。     

胰十二指肠切除术的技术改进

目的 探讨改进胰十二指肠切除术,预防术后并发症,提高手术疗效的方法。方法 采用保留幽门、胰管空肠粘膜吻合＋胰肠遮盖套入式吻合、胰管支撑外流充分切除胰钩突的术式,并观察其疗效。结果 全组未发生胰瘘及胰断面出血。保留幽门胰十二批肠切除术（ＰＰＰＤ）者有１例术后发生胃潴留,其余胃排空正常。结论 ＰＰＰＤ只要操作得当,可避免术后胃潴留。胰肠遮盖套入式吻合操作简便,可防止术后胰瘘、胰断面出血等并发症。     

基因表达谱芯片在胰腺癌相关基因筛选中的应用研究

目的：探讨基因表达谱芯片技术在高通量筛查肿瘤相关基因群及研究胰腺癌分子病理变化中的应用价值。方法：应用含有４０９６条人类全长基因的ｃＮＤＡ表达谱芯片,对３例临床切除的胰腺癌及正常胰腺标本的基因表达谱进行分析。结果：在３例胰腺癌和正常胰腺组织中均有差异表达的基因３９８条,其中新基因２８９条,老基因１０９条。从老基因中筛选出有显著表达差异基因３７条,其中在胰腺癌组织中上调基因２０条,下调基因１７条。结     

血清CA19-9,CA-50,CEA联合检测在胰腺癌诊断中的应用

目的:探讨血清CA19-9,CA-50,CEA联合检测对胰腺癌的诊断价值。方法:采用酶联免疫测定法和CA-50抗原免疫放射分析法对27例胰腺癌、19例肝癌和37例胃肠癌、30例消化道良性疾病患者血清CA-19、CA-50和CEA水平进行测定,并对胰腺癌、肝癌、胃肠癌及消化道良性疾病患者血清三项标志物的水平进行比较。结果:消化道恶性肿瘤组的血清CA19-9、CA-50、CEA水平明显高于消化道良性疾病组(P<005),尤以胰腺癌为著(P<001)。还发现肿瘤三项标志物联合测定阳性者(CEA>12ng/ml、CA19-9>37u/ml、CA-50>20u/ml三项中两项超过正常值或单项超过其两倍以上者)胰腺癌组占8889%,与其单检阳性率(4444%)相比有显著性差异(P<0005)。肝癌与胃肠癌两组的肿瘤标志物联检阳性率与单检阳性率相比均无显著性差异(P>005)。结论:血清CA19-9、CA-50和CEA联合检测对胰腺癌的诊断有重要价值。可明显提高胰腺癌的确诊率     

胞嘧啶脱氨基酶/5-氟胞嘧啶系统对人胰腺癌细胞恶性增殖的抑制作用

目的　探讨大肠杆菌胞嘧啶脱氨基酶 (CD) / 5 -氟胞嘧啶 (5 - FC)系统对人胰腺癌细胞的体内外生长抑制作用。方法　将含 CD基因的重组逆转录病毒载体导入人胰腺癌细胞形成转化细胞系 ,对转化细胞进行体内外药物敏感实验 ,包括 :(1)计算转化细胞在前体药物 5 - FC作用下的细胞生长抑制率和克隆形成抑制率 ;(2 )MTT法检测旁观者效应 ;(3)观察 5 - FC对转化细胞裸鼠移植瘤的抑制作用。结果　转化细胞在 5 - FC作用下其生长抑制率为 80 .0 % ,克隆形成抑制率为 79.0 % ,均明显高于未转化细胞生长抑制率 4.8%和克隆形成抑制率5 .0 % (P<0 .0 1) ;混合细胞中含 10 %的转化细胞时 ,生长抑制率已达 5 0 .7% ;转化细胞的裸鼠移植瘤在 5 - FC作用下体积缩小。结论　 CD/ 5 - FC系统对人胰腺癌细胞系细胞具有实验性基因治疗作用     

Interactions between imidazoline compounds and sulphonylureas in the regulation of insulin secretion

1. Imidazoline α₂-antagonist drugs such as efaroxan have been shown to increase the insulin secretory response to sulphonylureas from rat pancreatic B-cells. We have investigated whether this reflects binding to an islet imidazoline receptor or whether α₂-adrenoceptor antagonism is involved.
2. Administration of (±)-efaroxan or glibenclamide to Wistar rats was associated with a transient increase in plasma insulin. When both drugs were administered together, the resultant increase in insulin levels was much greater than that obtained with either drug alone.
3. Use of the resolved enantiomers of efaroxan revealed that the ability of the compound to enhance the insulin secretory response to glibenclamide resided only in the α₂-selective-(+)-enantiomer; the imidazoline receptor-selective-(−)-enantiomer was ineffective.
4. In vitro, (+)-efaroxan increased the insulin secretory response to glibenclamide in rat freshly isolated and cultured islets of Langerhans, whereas (−)-efaroxan was inactive. By contrast, (+)-efaroxan did not potentiate glucose-induced insulin secretion but (−)-efaroxan induced a marked increase in insulin secretion from islets incubated in the presence of 6 mM glucose.
5. Incubation of rat islets under conditions designed to minimize the extent of α₂-adrenoceptor signalling (by receptor blockade with phenoxybenzamine; receptor down-regulation or treatment with pertussis toxin) abolished the capacity of (+)-and (±)-efaroxan to enhance the insulin secretory response to glibenclamide. However, these manoeuvres did not alter the ability of (±)-efaroxan to potentiate glucose-induced insulin secretion.
6. The results indicate that the enantiomers of efaroxan exert differential effects on insulin secretion which may result from binding to effector sites having opposite stereoselectivity. Binding of (−)-efaroxan (presumably to imidazoline receptors) results in potentiation of glucose-induced insulin secretion, whereas interaction of (+)-efaroxan with a second site leads to selective enhancement of sulphonylurea-induced insulin release.

     

Preservation of the pylorus during pancreaticoduodenectomy —Evolution and current indications

The Whipple procedure has been improved by preservation of afunctioning pylorus. A functioning pylorus is important because marginal ulceration is avoided and, compared to the standard Whipple procedure with hemigastrectomy, more patients can gain weight postoperatively. The most common indications for this procedure are severe complication of chronic pancreatitis and periampullary tumors. In patients with pancreatic adenocarcinoma, the pylorus-preserving variety results in equal or better survival rates than those of the standard Whipple procedure with hemigastrectomy. Surgery alone is not sufficient to improve survival rates in patients with adenocarcinoma of the pancreas. Improved imaging modalities are required to diagnose the disease earlier. The most likely combination of treatment to prolong survival time is a combination of resection for cure in a patient with an early diagnosis plus an aggressive adjuvant chemoradiotherapy protocol. This protocol is most likely to be completed if a patient has preserved endocrine, exocrine, and digestive ability. A radical (R1) pylorus-preserving Whipple procedure would have the following advantages to result in the best survival rates — the patients can gain weight and thereby withstand the chemoradiotherapy protocol while, at the same time, the weakest aspect of the radical resection is addressed, i.e., the retroperitoneal margin of the pancreatic head.     

胰腺癌 P16、 P53及 PCNA 的表达及其临床意义

目的：研究胰腺癌中 Ｐ１６和 Ｐ５３基因产物的表达及其临床意义。方法：应用免疫组化 Ｌ Ｓ Ａ Ｂ法研究２８例胰腺癌组织中 Ｐ１６蛋白和 Ｐ５３蛋白的表达情况,并进行增殖细胞核抗原（ Ｐ Ｃ Ｎ Ａ）检测,计算细胞增殖指数（ Ｐｒｏｌｉｆｅｒａｔｉｏｎ ｉｎｄｅｘ, Ｐ Ｉ）。结果： Ｐ１６蛋白低表达和 Ｐ５３蛋白过表达均有促进胰腺癌细胞增殖的作用。 Ｐ１６蛋白表达与淋巴结转移无关; Ｐ５３蛋白高表达者具有较高的淋巴结转移率,预后较差。 Ｐ１６蛋白低表达与 Ｐ５３蛋白高表达共存者,其恶性度最高,预后最差。结论：联合检测 Ｐ１６和 Ｐ５３蛋白表达情况,更能充分反映胰腺癌的生物学行为,对胰腺癌患者预后判断及临床治疗有指导意义。     

Prevention and suppression of autoimmune pancreatic Beta-cell destruction in BB rats by syngeneic lymphocytes obtained from long-term normoglycaemic donors

Summary To prove whether a cell-mediated mechanism is responsible for maintaining long-term normoglycaemia in BB/OK rats with a proved immune attack (insulitis, reduced Beta-cell volume), we transferred lymphocytes obtained from those rats into normoglycaemic diabetes-prone BB/OK rats or into diabetic BB/OK rats receiving a simultaneous syngeneic islet graft. Our results show the presence of a lymphocyte population in the long-term normoglycaemic BB/OK rats, which is able to arrest pancreatic Beta-cell destruction in diabetes-prone BB/OK rats detected by a decreased diabetes incidence following single lymphocyte transfusion. Syngeneic islets were destroyed by recurrence of the autoimmune process when transplanted into diabetic BB/OK rats. Lymphocytes obtained from long-term normoglycaemic BB/OK rats were able to protect the syngeneic BB/OK islet graft from autoimmune destruction in diabetic BB/OK rats, whereas allogeneic islet destruction was not prevented. The phenotype of the effective lymphocyte population is not yet clear, but it is negative for RT6. We conclude that the mechanism responsible for maintaining normoglycaemia in long-term normoglycaemic BB/OK rats is cell mediated, because this property can be transferred to prevent autoimmune destruction of pancreatic Beta cells.