Gallbladder carcinoma: the role of p53 protein overexpression and Ki-67 antigen expression as prognostic markers

BackgroundThe overexpression of p53 protein and the expression of Ki-67 antigen may affect the survival of patients with gallbladder carcinoma. This association has been tested in a series of 41 patients with relatively early carcinoma of the gallbladder.MethodsForty-one surgical specimens from patients with a postoperative histological diagnosis of gallbladder carcinoma were studied. All patients were operated by simple cholecystectomy only because the tumours were not advanced and/or their general condition was poor. Patients submitted to radical operations were excluded. p53 expression was calculated from nuclear staining according to the intensity and extent of positive cells, as graded on a scale from 1 to 3; a combined score of >3 was considered as overexpression. Ki-67 expression was calculated by the MIB-I index: the percentage of positively stained tumour cell nuclei out of the total tumour cells counted (n = 1000); >20% of stained cells was considered positive.ResultsTwenty-nine gallbladder carcinomas (71%) overexpressed p53 protein in the cell nuclei. No significant differences were found in relation to cell differentiation on the level of tumour infiltration through the gallbladder wall. Five-year survival of patients with gallbladder carcinoma overexpressing p53 was 17.2%, while survival of patients without p53 overexpression was 30% (not significant). Twenty-four cases (58.5%) were considered positive for the MIB-I index. There were no differences between the grade of cell differentiation and wall infiltration. Five-year survival of the patients with a MIB-I positive index was 9.2% as opposed to 27.7% for those with a negative index (not significant).Conclusionsp53 protein nuclear overexpression and Ki-67 protein expression in gallbladder carcinoma were not related to histological differentiation, level of gallbladder wall invasion or patient survival.     

Expression of p57(kip2) and its relationship with clinicopathology, PCNA and p53 in primary hepatocellular carcinoma

AIM: To investigate the expression of p57kip2 and its relationship with clinicopathology, PCNA and p53 in primary hepatocellular carcinoma (HCC). METHODS: Expression of p57kip2, PCNA and p53 in tumor tissues from 32 patients with HCC and 10 liver tissues of normal persons was detected with Elivision immunohistochemical technique. RESULTS: The p57kip2 protein positive-expression rate in HCC was 56.25%, lower than that in normal tissues (100%, P<0.05). The reduced expression of p57kip2 protein correlated significantly with moderate or low differentiation of tumor cells (P = 0.007 <0.05), high clinical stage (P= 0.041 <0.05) and poor prognosis (P= 0.036 <0.05), but did not correlate significantly with metastasis, tumor size, level of AFP and age (P>0.05). The PCNA positive-expression rate was 56.25%, which was correlated significantly with the expression of p57kip2 (P= 0.025<0.05). The p53 positive-expression rate was 46.88%, which was not correlated significantly with the expression of p57kip2 (P>0.05). CONCLUSION: There is a marked loss or absence of p57kip2 expression and high expression of PCNA in HCC, which are involved in carcinogenesis and development of HCC. The p57kip2 and p53 may induce apoptosis via different mechanisms.     

p53、Ki-67基因表达与膀胱癌生物学特性的研究

目的 探讨p53、Ki-67基因表达与膀胱移行细胞癌(BTCC)病理分级、临床分期及复发的关系.方法 收集149例BTCC患者的临床资料及p53、Ki-67表达阳性率.结果 Ⅰ～Ⅱ级BTCC p53、Ki-67阳性率分别为58.8%、64.7%,低于Ⅲ级BTCC p53、Ki-67的阳性率(80.014%、90.0%)(P<0.05,P<0.01);浸润型BTCC的p53、Ki-67基因表达阳性率(80.0%、92.3%)均高于浅表型BTCC阳性率(50.0%、52.4%)(P<0.01).在高分级、高分期BTCC组p53、Ki-67联合表达率(73.3%、73.8%)高于低分级、低分期BTCC组(45.4%、32.1%)(P<0.05).p53、Ki-63共同表达阳性者复发率为37.2%,单一阳性或阴性表达者复发率16.1%,两组复发率有显著性差异(P<0.05).结论 p53、Ki-67基因表达与BTCC的临床分期、病理分级相关,提示p53、Ki-67蛋白过度表达的BTCC高度恶性和预后不良;p53、ki-67基因共同表达阳性组复发率较单一阳性或阴性组复发率高,提示p53和ki-67基因联合表达与BTCC复发可能有相关性.     

p62-containing,proteolytically active nuclear condensates,increase the efficiency of the ubiquitin–proteasome system

Degradation of a protein by the ubiquitin–proteasome system (UPS) is a multistep process catalyzed by sequential reactions. Initially, ubiquitin is conjugated to the substrate in a process mediated by concerted activity of three enzymes; the last of them—a ubiquitin ligase (E3)—belongs to a family of several hundred members, each recognizing a few specific substrates. This is followed by repeated addition of ubiquitin moieties to the previously conjugated one to generate a ubiquitin chain that serves as a recognition element for the proteasome, which then degrades the substrate. Ubiquitin is recycled via the activity of deubiquitinating enzymes (DUBs). It stands to reason that efficiency of such a complex process would depend on colocalization of the different components in an assembly that allows the reactions to be carried out sequentially and processively. Here we describe nuclear condensates that are dynamic in their composition. They contain p62 as an essential component. These assemblies are generated by liquid–liquid phase separation (LLPS) and also contain ubiquitinated targets, 26S proteasome, the three conjugating enzymes, and DUBs. Under basal conditions, they serve as efficient centers for proteolysis of nuclear proteins (e.g., c-Myc) and unassembled subunits of the proteasome, suggesting they are involved in cellular protein quality control. Supporting this notion is the finding that such foci are also involved in degradation of misfolded proteins induced by heat and oxidative stresses, following recruitment of heat shock proteins and their associated ubiquitin ligase CHIP.

An important, yet unsolved question is how cells recruit the appropriate reactants involved in biochemical reactions, to a defined location at a specific time to increase the reaction efficiency and processivity. This is particularly relevant for sequential transformations along cascades that are catalyzed by different enzymes and complexes, such as degradation of a protein by the ubiquitin–proteasome system (UPS). Separation of the interior milieu of membrane-bound organelles (e.g., nucleus, Golgi apparatus, endoplasmic reticulum, mitochondria, and lysosomes) from the surrounding environment enables the cells to control the spatial distribution of specific reactions and their components. However, this compartmentalization makes it difficult to allow exchange of components necessary for providing high specificity, for example. In addition, cells contain supramolecular assemblies that are not bound by surrounding membranes and can be found both in the cytoplasm (such as the centriole, P bodies, and stress granules) and the nucleus (such as nucleoli, promyelocytic leukemia [PML] bodies, Cajal bodies, and nuclear speckles) (1, 2).Emerging evidence shows that many membraneless biomolecular condensates are formed by liquid–liquid phase separation (LLPS) (3). These condensates provide a different environment from the surrounding cytoplasm or nucleoplasm and probably have an important role in the concentration of biomolecules, thus allowing efficient multistep processes to occur. In addition, it allows for rapid exchange of specific components—such as ubiquitin ligases—to occur and thus allowing accommodation to changing pathophysiological conditions and the requirement for high specificity of different processes. Recently, it was shown that p62, also known as Sequestosome-1 (SQSTM-1), forms spherical liquid-like condensates (bodies) both in the cytosol and in a cell-free system (4). Formation of these condensates is mediated by the ability of the protein to oligomerize into helical filaments through its N-terminal PB1 (Phox and Bem1) domain, and to bind ubiquitin (Ub) chains attached to target substrates via its C-terminal UBA (ubiquitin-associated) domain (5). The efficiency of p62 condensate formation was shown to be strongly dependent on the length of the Ub chains attached to the substrates (6).Cytosolic p62 condensates play an important role in maintaining protein homeostasis and quality control by their ability to sequester ubiquitinated proteins and shuttle them for degradation by the autophagy–lysosome system. This is mediated via direct interaction of the p62’s LIR motif with the autophagosome-incorporated LC3 (7). In addition to its role in autophagy, p62 was shown to deliver cytosolic ubiquitinated substrates to the proteasome, by direct interaction of its PB1 domain with the 19S Rpn1 and Rpn10 proteasomal subunits (8).p62 is widely distributed in the cell, and its nucleocytoplasmic shuttling is mediated by two nuclear localization signals (NLS1 and NLS2) and one nuclear export signal (NES) (9). In addition to its cytosolic functions, p62 forms nuclear bodies that exist both as separate and as hybrid structures by interacting with PML or Cajal bodies (10). Since autophagy occurs exclusively in the cytosol, the role and biological significance of nuclear p62 have remained elusive.In the present study we show that p62 is involved in the formation of nuclear LLP-separated foci, which recruit components of the UPS and protein substrates, resulting in their efficient degradation under both basal and stressed conditions.     

人类端粒酶逆转录酶hTERT Ki-67及p27kip1在嗜铬细胞瘤组织的表达及意义研究

目的研究人端粒酶逆转录酶(hTERT)、Ki-67及p27kip1的表达在嗜铬细胞瘤发生与发展中的作用和作为预测生物学行为标志物的价值。方法采用免疫组织化学方法检测hTERT、Ki-67及p27kip1在2000—2004年广西医科大学第一附属医院病理科的45例嗜铬细胞瘤和神经节细胞瘤及9例正常肾上腺组织中的表达。结果hTERT蛋白的表达在良性(3/31例)和可疑恶性(6/7例)以及良性与恶性肿瘤(5/7例)间的差异均有统计学意义(P<0.01)。31例良性肿瘤中26例未检测到Ki-67,而恶性肿瘤和可疑恶性肿瘤均为阳性;Ki-67与hTERT的表达呈正相关性(r=0.544,P<0.01)。恶性和可疑恶性肿瘤中未检测到p27kip1,5例良性肿瘤为阳性,所有正常肾上腺髓质标本均可检测到p27kip1的表达。p27kip1与hTERT的表达无相关性。结论端粒酶的激活在恶性嗜铬细胞瘤和神经节细胞瘤的发生发展中起着重要作用,在细胞周期调控中端粒酶可能存在不同的激活途径。hTERT和Ki-67的检测可作为鉴别良恶性嗜铬细胞瘤的手段。     

肝癌组织中p62~（c－myc）表达及其意义

应用免疫组织化学（ＡＢＣ法）技术对４８例原发性肝癌患者的肝癌及癌旁石蜡包埋组织中ｐ６２~（ｃ－ｍｙｃ）进行检测，结果显示ｐ６２~（ｃ－ｍｙｃ）的阳性率在肝癌中为８３．３％（４０／４８），在癌旁组织为８９．６％（４３／４８），说明ｃ－ｍｙｃ基因的激活与肝癌癌变过程有密切关系。同时对ｐ６２~（ｃ－ｍｙｃ）表达的意义进行了讨论。     

TIMP-1和TIMP-2在原发性肝癌生长、浸润及转移中的作用

目的：了解基质金属蛋白酶组织抑制因子-1(tissue inhibitou of metalloproteinase-1，TIMP-1)和基质金属蛋白酶组织抑制因子-2(TIMP-2)mRNA及相关抗原在肝癌组织中的定位和表达状态，探讨TIMP-1和TIMP-2在肝癌组织生长、浸润及转移中所起的作用。方法：以TIMP-1和TIMP-2探针及单克隆抗体（McAb）为试剂，采用原位杂交技术及免疫组织化学法检测原发性肝癌、肝高分化腺癌的肝组织中TIMP-1和TIMP-2mRNA及相关抗原的表达，并与10例正常肝组织做对照。结果：20例原发性肝癌患者的肝组织中TIMP-1和TIMP-1mRNA及相关抗原表达的阳性率为90%;9例肝高分化腺癌的腺癌组织中无TIMP-1和TIMP-2mRNA及相关抗原的表达；10例正常肝组织中TIMP-1和TIMP-2mRNA及相关抗原表达均为阴性；TIMP-1和TIMP-2mRNA及相关抗原阳性信号呈现为棕黄色颗粒状，分布在肝细胞浆内，未见细胞核着色；无论是原发性肝癌癌组织还是癌周组织中,TIMP-1的表达强于TIMP-2的表达，癌周组织中TIMP-1和TIMP-2mRNA和相关抗原的表达与肝组织病理改变相关，即肝硬化者表达强，慢性肝炎者表达弱，正常肝组织无表达。结论：原发性肝癌的癌组织中存在TIMP-1和TIMP-2mRNA及相关抗原的表达，其表达强度可能与原发性肝癌的分型有关，它可能通过抑制MMP的活性使ECM降解减少从而阻止癌细胞通过基底膜移出而抑制肝癌细胞向周围浸润及转移。     

人类端粒酶逆转录酶hTERT Ki-67及p27^kipl在嗜铬细胞瘤组织的表达及意义研究

目的 研究人端粒酶逆转录酶（hTERT）、Ki-67及p27^kipl的表达在嗜铬细胞瘤发生与发展中的作用和作为预测生物学行为标志物的价值。方法 采用免疫组织化学方法检测hTERT、Ki-67及p27^kipl在2000-2004年广西医科大学第一附属医院病理科的45例嗜铬细胞瘤和神经节细胞瘤及9例正常肾上腺组织中的表达。结果 hTERT蛋白的表达在良性（3／31例）和可疑恶性（6／7例）以及良性与恶性肿瘤（5／7例）间的差异均有统计学意义（P〈0.01）。31例良性肿瘤中26例未检测到Ki-67，而恶性肿瘤和可疑恶性肿瘤均为阳性；Ki-67与hTERT的表达呈正相关性（r=0．544，P〈0．01）。恶性和可疑恶性肿瘤中未检测到p27^kipl，5例良性肿瘤为阳性，所有正常肾上腺髓质标本均可检测到p27^kipl的表达。p27^kipl与hTERT的表达无相关性。结论 端粒酶的激活在恶性嗜铬细胞瘤和神经节细胞瘤的发生发展中起着重要作用，在细胞周期调控中端粒酶可能存在不同的激活途径。hTElit和Ki-67的检测可作为鉴别良恶性嗜铬细胞瘤的手段。     

Expression of Ki-67, p53, and K-ras in chronic pancreatitis and pancreatic ductal adenocarcinoma

AIM: To examine surgical specimens of pancreas with either chronic pancreatitis or pancreatic cancer in order to study whether ductal hyperplasia and dysplasia in pancreas represent precursor lesions for pancreatic cancer. METHODS: We examined expression of Ki-67, CEA, p53, and K-ras, in the surgical specimens of pancreas with adenocarcinomas (n= 11) and chronic pancreatitis (n = 12). Cellular proliferation was assessed by Ki-67 proliferation index using the proliferation marker Ki-67. In specimens with pancreas cancer, we divided pancreas epithelium into normal (n = 7), ductal hyperplasia (n = 3), dysplasia (n = 4), and cancerous lesion (n = 11) after hematoxylin and eosin staining, Ki-67, and CEA immunohistochemical staining. In cases with chronic pancreatitis, the specimen was pathologically examined as in cases with pancreas cancer, and they were also determined as normal (n = 10), ductal hyperplasia (n = 4), or dysplasia (n = 5). p53 and K-ras expression were also studied by immunohistochemical staining. RESULTS: In pancreatic cancer, the Ki-67 index was 3.73±3.58 in normal site, 6.62±4.39 in ductal hyperplasia, 13.47±4.02 in dysplasia and 37.03±10.05 in cancer tissue, respectively. Overall, p53 was positive in normal ducts, ductal hyperplasia, dysplasia, and carcinoma cells in 0 of 14 (0%), 0 of 7(0%), 7 of 9 (78%), and 10 of 11 (91%), respectively, and K-ras was positive in 0 of 8 (0%), 1 of 3 (33%), 4 of 6 (67%), 4 of 5 (80%), respectively. CONCLUSION: Our results favorably support the hypothesis that ductal hyperplasia and dysplasia of the pancreas might be precursor lesions for pancreas cancer. Further evaluation of oncogenes by the molecular study is needed.     

胰腺癌组织中SATB1和Ki-67的表达变化及意义

目的 观察核基质结合区结合蛋白1（SATB1）和Ki-67在胰腺癌组织中的表达变化,并探讨其意义.方法 应用免疫组化SP法检测58例胰腺癌组织、配对癌旁组织及正常胰腺组织中SATB1和Ki-67的表达,将二者在胰腺癌中的表达水平与临床病理参数的关系进行统计学分析.结果 SATB1和Ki-67在胰腺癌中的阳性表达率分别为63.8％ （37/58）、70.7％ （41/58）,且在胰腺癌、癌旁组织及正常组织中的表达呈下降趋势.胰腺癌组织中SATB1的表达与患者年龄、T分期、淋巴结转移和TNM分期相关（P＜0.05）,Ki-67的表达与T分期、淋巴结转移和TNM分期相关（P＜0.05）.Cox分析显示,SATB1（RR=18.625,95％ CI为11.178 ～ 285.631）和Ki-67（RR=1.985,95％ CI为0.394～ 320.525）是影响胰腺癌患者预后的独立因素（P均＜0.05）.结论 SATB1和Ki-67在胰腺癌组织中高表达,可作为胰腺癌发生发展的预测指标之一.     

p53 point mutations in primary human gastric carcinomas

Summary p53 point mutations in primary gastric carcinomas were analyzed by performing cDNA deoxynucleotide sequencing of the gene. Out of 16,9 (56.3%) primary gastric carcinoma cases, including early cancer, showed one or more p53 point mutations in their open-reading frame, and 4 out of 9 cases had a p53 point mutation within highly conserved domains. The characteristics of the p53 mutation spectrum observed in primary tumors were (a) frequent mutation at an A:T pair (50%, 7 out of 14 mutations), (b) high transversion incidence (29%, 4 out of 14 mutations), (c) no transition at CpG, and (d) no G:C to T:A transversion. Our results suggest that p53 mutation is a common event in gastric carcinoma occurring from the early stage of progression with its specific mutation spectrum.Abbreviation PCR-SSCP polymerase chain reaction single-strand conformation polymorphism     

胰腺癌组织Survivin与Ki-67的表达及其意义

目的:探讨Survivin和Ki-67在胰腺癌组织中的表达及其与临床病理特征的关系．方法:采用免疫组织化学技术检测各期胰腺癌86例及癌旁组织78例中Survivin和Ki-67的表达水平,并结合病理特征进行分析。结果:胰腺癌旁组织或良性肿瘤旁组织不表达Survivin 蛋白．胰腺癌组织Survivin阳性表达率为87．9％,显著高于胰岛细胞癌(12．7％)或胰岛细胞瘤(5．2％)(P<0．01),而且Survivin表达程度与肿瘤分化程度、淋巴结转移相关(P<0．05)．Ki-67蛋白在胰腺癌组织中阳性表达率为 94．4％,显著高于胰岛细胞癌或胰岛细胞瘤组(P<0．01), 并与胰腺癌组织分化程度相关(P<0．05)．两种蛋白表达有高度相关性(r=0．87)．结论:Survivin和Ki-67在胰腺癌组织中过表达,并且与胰腺癌病理特征密切相关．Survivin可能是反应胰腺癌预后不良的指标．     

内镜下支架置入术治疗消化道狭窄273例

目的:探讨内镜下支架置入术治疗消化道狭窄的临床疗效、安全性及患者的治疗满意度.方法:273例消化道狭窄患者,食管贲门狭窄242例,胃十二指肠狭窄24例,结肠直肠狭窄7例;恶性狭窄256例,良性狭窄17例,所有患者均有不同程度的消化道梗阻症状,其中15例合并食管气管瘘,均行内镜直视下支架置入术,术后观察临床疗效和不良反应...     

E-钙黏蛋白和Ki-67在非特殊型乳腺浸润性导管癌中的表达及意义

目的探讨E-钙黏蛋白和增殖指数抗原Ki-67在非特殊型乳腺浸润性导管癌发生、发展中的作用。方法采用免疫组化法检测E-钙黏蛋白和Ki-67在100份非特殊型乳腺浸润性导管癌组织（乳腺癌组）及20份乳腺纤维腺瘤组织（纤维腺瘤组）中的表达,并分析两者与非特殊型乳腺浸润性导管癌临床病理特征的关系。结果乳腺癌组E-钙黏蛋白的阳性率（67%）明显低于纤维腺瘤组（100%）,Ki-67的阳性率（59%）高于纤维腺瘤组（25%）,P均〈0.05;E-钙黏蛋白和Ki-67表达与非特殊型乳腺浸润性导管癌淋巴结转移、TNM分期、组织学分级密切相关,与患者年龄、肿瘤直径无明显相关性。结论 E-钙黏蛋白表达降低、Ki-67表达升高与非特殊型乳腺浸润性导管癌的发生、发展密切相关,检测两者有助于判断非特殊型乳腺浸润性导管癌的恶性程度及预后。     

Apoptosis and cell proliferation in the development of gastric carcinomas: associations with c-myc and p53 protein expression

BACKGROUND AND AIM: Patients with gastric carcinomas have a poor prognosis and low survival rates. The aim of the present paper was to characterize cellular and molecular properties to provide insight into aspects of tumor progression in early compared with advanced gastric cancers. METHODS: One hundred and nine graded gastric carcinomas (early or advanced stage, undifferentiated or differentiated type) with paired non-cancer tissue were studied to define the correlation between apoptosis (morphology, terminal deoxyribonucleotidyl transferase-mediated dUTP-digoxigenin nick end-labeling), cell proliferation (Ki-67 expression, morphology) and expression and localization of two proteins frequently having altered expression in cancers, namely p53 and c-myc. RESULTS: Overall, apoptosis was lower in early stage, differentiated and undifferentiated gastric carcinomas compared with advanced-stage cancers. Cell proliferation was comparatively high in all stages. There was a high level of p53 positivity in all stages. Only the early- and advanced-stage undifferentiated cancers that were p53 positive had a significantly higher level of apoptosis (P < 0.05). Cell proliferation was significantly greater (P < 0.05) only in the early undifferentiated cancers that had either c-myc or p53-positivity. CONCLUSIONS: The results indicate that low apoptosis and high cell proliferation combine to drive gastric cancer development. The molecular controls for high cell proliferation of the early stage undifferentiated gastric cancers involve overexpression of both p53 and c-myc. Overexpression of p53 may also control cancer development in that its expression is associated with higher levels of apoptosis in early and late-stage undifferentiated, cancers.     

肝细胞癌组织HSP70、p53和PCNA的表达及其意义

目的探讨热休克蛋白70（HSP70）、p53和增殖细胞核抗原（PCNA）在肝细胞癌（HCC）组织中的表达及其意义。方法采用免疫组化法检测正常人、慢性乙型肝炎、肝硬化和HCC肝或癌组织HSP70、p53和PCNA的表达情况。结果 HCC组织HSP70、p53和PCNA表达阳性率明显高于非癌组织（x1^2=27.16x2^2=67.6,x3^2=40.6,P〈0.01）;HSP70在正常人、慢性乙型肝炎、肝硬化和HCC中的表达逐步增强;HSP70和p53在分化较好的HCC中的阳性率明显低于分化不良者（x1^2=6.8,P1〈0.01x2^2=6.1,P2〈0.05）,而PCNA表达与HCC组织分化程度无关（x2=2.4,P〉0.05）;HSP70表达强度与p53和PCNA表达关系密切（x1^2=41.3,x2^2=41.4,P〈0.01）。结论 HCC是HSP70高表达肿瘤。HSP70表达与p53和PCNA表达密切相关,因而在HCC发生和发展中起重要作用。     

Expression of IGFBP2 in Gastric Carcinoma and Relationship With Clinicopathologic Parameters and Cell Proliferation

The insulin-like growth factor (IGF) axis is a complex system composed of two mitogenic ligands, IGF-I and IGF-II, two receptors, IGF-IR and IGF-IIR, and six binding proteins, IGFBP1 to IGFBP6. The IGFBPs exert their actions through their regulation of IGF bioavailability for IGF receptors. The present study evaluated the correlation between IGFBP2 expression and clinicopathologic parameters and cell proloferation in cancer by using surgically resected tissue specimens from 97 patients with gastric carcinoma treated at our hospital. Immunohistochemical staining was performed using IGFBP2 and Ki-67 monoclonal antibody. An obvious difference existed in the IGFBP2 expression between carcinomas and normal mucosa. Correlation between IGFBP2 expression and the depth of penetration, lymph node metastasis, and clinical stage were observed. There was positive correlation between IGFBP2 expression and Ki-67 expression. We conclude that IGFBP2 may be involved in carcinogenesis and progression of gastric carcinoma by promoting cell proliferation.     

善得定治疗癌性上消化道出血临床观察

目的为观察善得定治疗恶性肿瘤所致上消化道出血的疗效及副作用方法选用恶性肿瘤所致上消化道出血６６例，随机分为善得定治疗组和垂体后叶素对照组，治疗组病人先用善得定０１ｍｇ＋０．９％ＮＳ２０ｍｌ静推，后用善得定以每小时２５微克滴速静滴维持２４～４８小时，对照组用垂体后叶素以每小时２～５Ｕ滴速静滴维持２４～４８小时，同时给硝酸甘油０．５ｍｇ吞下含服。结果治疗组总有效率为８８２３％（３０／３４），对照组总有效率为６２５０％（２０／３２），两组差异有显著意义（Ｐ＜００５），治疗组每例平均输血量为７００８０±３２７１８ｍｌ，对照组输血量平均每例为１１７６００±３２４１２ｍｌ，两组差异显著（Ｐ＜０００１）。两组均无严重副作用。结论癌性上消化道出血是晚期肿瘤常见并发症及致死原因之一，善得定较传统的垂体后叶素治疗具有止血快、止血率高，副作用少等优点，且可减少输血量，值得临床广泛推广使用。     

急性心肌梗死患者HbA1c与高敏C反应蛋白、CD62p、纤维蛋白原的关系

目的观察急性心肌梗死患者HbA1c与CD62p、纤维蛋白原（Fib）与炎性因子高敏C反应蛋白（hsc-RP）的关系。方法对象选自2008年1月至2009年3月,年龄45-85岁,符合急性心肌梗死诊断标准的入院患者96例。测定HbA1c、Fib、CD62p与hsC-RP。同时随访6个月后的临床终点事件的发生率及这些指标和临床终点事件的相关性。结果根据HbA1c水平将急性心肌梗死（AMI）患者分为HbA1c增高组（35例）及HbA1c正常组（61例）。HbA1c增高组血小板CD62p、hsC-RP、Fib显著高于HbA1c正常组（P〈0．05）。此外,所有AMI患者HbA1c水平与hsC-RP呈正相关（r=0．37,P〈0．01）;所有AMI患者血小板CD62p与hsC-RP呈正相关（r=0．43,P〈0．01）。HbA1c增高组出现临床终点事件者5例,包括随访6月内的再发AMI,再住院行心肌血管重建术、住院期间及随访期间的心源性死亡者;HbA1c正常组未出现临床终点事件。随访6个月内出现临床终点事件者（5例）与无心脏事件（89例）相比,左室射血分数（P〈0．01）、血hsC-RP（P〈0．05）为影响临床终点事件的因素。结论HbA1c水平可能是影响急性心肌梗死患者病情发展及预后的重要因素。