幽门螺杆菌感染与胃癌、慢性胃炎、溃疡病、异型增生的关系及PCNA表达

目的　探讨幽门螺杆菌 (Hp)感染的不同胃黏膜增殖性病变的演进中增殖细胞核抗原 (PCNA)的表达及其意义。方法　对 13 0例病理证实的不同胃黏膜病变应用免疫组化方法检测 PCNA标记指数 (L I) ,Warthin-starry法检测 Hp感染。结果　 PCNA -L I在浅表性胃炎为 2 2 .0 0± 16.95,萎缩肠化性胃炎为 46.45± 19.10 ,溃疡病为 45.75± 18.15,异型增生为 61.0 6± 2 0 .67。在萎缩肠化性胃炎、溃疡病、异型增长及胃癌组织中均高于浅表性胃炎 (P<0 .0 5)。萎缩肠化型胃炎、溃疡病、异型增生及胃癌中 Hp感染阳性组 PCNA阳性表达均高于 Hp阴性组 (P<0 .0 5)。结论　 PCNA表达和 Hp感染与胃黏膜增殖和恶化有关     

细胞凋亡和细胞增殖在胃癌形成中的作用

目的 :探讨细胞凋亡和细胞增殖在胃癌发生发展中的作用。方法 :用原位末端标记法和免疫组织化学染色 ,检测 30例胃癌和 2 0例胃粘膜上皮异型增生中的细胞凋亡和调控基因 (Bcl 2 ,Fas)及增殖细胞核抗原 (PCNA)的表达情况。结果 :随正常胃粘膜胃粘膜异型增生胃癌的梯度 ,细胞凋亡指数(AI)逐渐降低 ,差异有显著性 (P <0 0 5) ;Bcl- 2的阳性表达率逐渐升高 ,Fas的阳性表达率逐渐降低 ,差异均有显著性 (P <0 .0 1) ,且二者有相关性 (P <0 0 5)。PCNA阳性表达率 (即增殖指数 ,PI)逐渐升高 (P <0 .0 1)。结论 :胃粘膜异型增生中已存在细胞凋亡和细胞增殖的异常 ,使增殖 /凋亡比值加大 ,是胃粘膜异型增生向胃癌发展的重要机制之一     

幽门螺杆菌感染与胃腺上皮细胞增生关系的研究

 目的:研究幽门螺杆菌(HP)与胃腺上皮细胞增生的关系, 方法:经PCR检测和组织病理学观察138例胃粘膜活检标本, 采用SP免疫组化染色观察PCNA表达和Feulgen二染色测定细胞核DNA含量。 结果:细胞核DNA含量在慢性浅表性胃炎(CSG)和慢性萎缩性胃炎(CAG)中, 有HP感染与无HP感染比较, 二倍体和近二倍体细胞减少, 增殖倍体增加。 PCNA表达在CSG和CAG中, 有HP感染与无HP感染比较阳性细胞数和均值增加。 结论:HP感染与胃腺上皮细胞的增生程度有密切关系。     

胃癌及癌前病变中p53蛋白表达与HP感染的关系

目的 观察幽门螺旋杆菌(HP)感染后胃癌、胃粘膜异型增生和胃粘膜肠化生中p53蛋白表达的特点,探讨HP在胃癌发生发展过程中的作用.方法 应用免疫组化SP法及美兰染色,对胃癌79例,胃粘膜异型增生23例,胃粘膜肠化生21例进行p53蛋白表达及HP检测并与56例慢性胃炎对比分析.结果 胃癌组、胃粘膜异型增生组及胃粘膜肠化生组的HP感染率及p53蛋白阳性表达率均明显高于慢性胃炎组(P＜0.05);122例HP阳性者p53蛋白表达80例,阳性率65.6%,58例HP阴性者p53蛋白表达5例,阳性率8.6%,两者比较,差异显著(P＜0.05).结论 在慢性胃炎、胃粘膜肠化生、胃粘膜异型增生、胃癌的进展过程中,p53蛋白的表达水平在增高.HP感染在胃癌发生、发展过程中起一定作用.p53蛋白的表达可能是HP致癌的作用机制之一.     

胃粘膜病变细胞增殖分级的研究

应用免疫组织化学方法检测２３０例胃粘膜病变标本中增殖细胞抗原的表达，计算细胞增殖指数，探讨细胞垃镇发级及其在胃癌发生中的意义。结果显示正常或慢性浅表性胃炎、伴肠化生慢性萎缩民生胃炎、伴异型增生慢笥萎缩性胃炎以主胃腺癌的ＬＩ逐渐增高，差异非常明显。     

胃癌及癌前病变与幽门螺杆菌感染相关性的临床分析

目的:测定幽门螺杆菌在萎缩肠化生胃炎,异型增生及胃癌中感染情况,探讨Hp与它们的相关性。方法:萎缩肠化生胃炎(A组)患者342例,异型增生(B组)229例,胃癌患者(C组)298例,采用Hp抗体ELISA法检测血清抗Hp-IgG抗体。结果:肠化生患者较非肠化生胃黏膜中的Hp感染多见。异型增生和胃癌的Hp感染率均高于萎缩性胃炎组(P<0.05),异型增生和胃癌两者间的Hp感染率亦存在差异(P<0.05)。幽门螺杆菌感染的萎缩肠化生胃炎及异性增生较非幽门螺杆菌感染者发生癌变的差异性显著,P<0.05;幽门螺杆菌感染的胃癌5年生存期显著短于非感染者,P<0.05。结论:Hp感染与萎缩肠化生胃炎,异型增生及胃癌有密切相关性,并缩短萎缩肠化生胃炎,异型增生癌变时间,缩短胃癌5年生存时间。     

胃粘膜上皮异型增生细胞增殖活性及凋亡与幽门螺杆菌感染的关系

背景与目的:异型增生是胃癌的癌前病变,但其癌变机制目前仍不清楚,本文通过对异型增生自然转归过程中细胞增殖活性和凋亡变化及幽门螺杆菌(Helicobacterpylori,HP)感染状态的研究,探讨二者之间的关系及其对异型增生癌变的影响。方法:取12例正常胃粘膜(对照组)和105例有随访结果的胃粘膜异型增生胃镜活检标本〔其中高度异型增生35例(癌变30例、未癌变5例);低度异型增生70例(癌变18例、未癌变52例)〕。全部标本均采用TUNEL(terminaldeoxynucleotidyltransferasemediatednickendlabeling)法检测凋亡情况;采用免疫组化法检测增殖细胞核抗原(proliferatingcellnuclearantigen,PCNA)表达情况;采用多聚酶链反应(polymerasechainreaction,PCR)检测HP及其CagA(+)株感染状况。结果:异型增生的HP感染率为84.76%,与对照组的83.33%相比差异无统计学意义,但CagA(+)株感染率为85.39%,高于对照组的60.00%。HP(+)和CagA(+)病例的增殖指数分别较HP(-)和CagA(-)为高(P<0.05),异型增生中PCNA的异常与HP及CagA(+)株感染有关(P<0.05)。凋亡/增殖比的变化与Hp的CagA(+)株感染有关(P<0.05)。结论:胃粘膜异型增生的形成及其自然转归过程中,异型增生的细胞动力学异常与HP、CagA(+)株感染有关。     

Survivin、PTEN、p53、Ki-67在胃癌前病变中的表达及相关性

目的 探讨凋亡抑制基因Survivin和抑癌基因PTEN、p53以及增殖核抗原Ki-67在胃癌及癌前病变组织中的表达及其相关性.方法 应用免疫组织化学SP法检测Survivin、PTEN、p53及Ki-67蛋白在10例正常胃黏膜组织、33例浅表性胃炎、30例萎缩性胃炎(无肠化)、33例萎缩性胃炎(伴肠化)、31例异型增生(轻度13例,中～重度18例)、25例胃癌中的表达.结果 Survivin、PTEN、p53及Ki-67蛋白在正常胃黏膜组织的阳性表达率分别为0%、100%、0%、0%,在浅表性胃炎的阳性表达率分别为0%、100%、0%、18%,在萎缩性胃炎(无肠化)中阳性表达率分别为0%、93%、0%、33%,在萎缩性胃炎(伴肠化)中阳性表达率分别为0%、91%、0%、39%.在轻度异型增生胃黏膜中的表达率分别为7%、77%、7%、54%,在中度异型增生胃黏膜中的表达率分别为20%、70%、30%、60%,在重度异型增生胃黏膜中的表达率分别为50%、63%、63%、75%,在胃癌组织中表达率分别为56%、60%、68%、88%.Survivin、p53在异型增生中和胃癌组织中有阳性表达,且二者在重度异型增生与胃癌组织间均无显著差异(P＞0.05).PTEN在各胃黏膜组织中均有表达,且表达率逐渐降低,其中异型增生与萎缩性胃炎及浅表性胃炎比较均有显著差异(P＜0.05),异型增生与胃癌组织之间无显著差异(P＞0.05).Ki-67在正常胃黏膜中不表达,在异型增生与胃癌组织间有显著差异(P＜0.05).在异型增生和胃癌组织中Survivin和p53蛋白的表达呈正相关(P＜0.05);与PTEN蛋白的表达呈负相关(P＜0.05);与Ki-67(Ⅲ～Ⅳ)表达呈正相关(P＜0.05).结论 Survivin、PTEN、p53、Ki-67蛋白在胃癌的发生、发展中起协同作用.对其进行联合检测有助于胃癌的早期诊断.     

PCNA在胃粘膜肠上皮化生、异型增生、和胃癌中的表达及意义

目的　观察增殖细胞抗原 (PCNA)在胃粘膜肠上皮化生、异型增生及胃癌中的表达情况 ,评估癌前病变的发展趋势。方法　免疫组织化学方法。结果　PCNA在细胞核内表达 ,从肠上皮化生、异型增生到胃癌呈递增趋势 ,在肠上皮化生表现为轻度表达 ,异型增生以中度为主 ,而胃癌多呈重度和过度表达。结论　PCNA在胃粘膜不同疾病细胞核内的表达 ,反映了细胞增殖状态和生长速度 ,有助于判断肠上皮化生、异型增生的发展趋势及胃癌的预后     

胃癌、癌前病变组织中p53蛋白表达的临床意义

目的探讨胃癌及癌前病变组织中p53蛋白表达的临床意义.方法采用间接免疫荧光标记染色和流式细胞术,检测并比较10例正常胃粘膜、13例浅表性胃炎、10例肠上皮化生、11例不典型增生及16例胃癌组织中p53蛋白的表达水平.以DNA指数、增殖指数(PI)、荧光指数(FI)为分析指标.结果胃癌、不典型增生及肠上皮化生的FI值分别为1.866±0.096、1.143±0.060、1.050±0.074,与正常胃粘膜(0.602±0.077)比较,均有显著性差异(P＜0.05),与浅表性胃炎(0.898±0.052)比较,也有显著性差异(P＜0.05).胃癌组织的FI值高于不典型增生及肠上皮化生(P＜0.05).不典型增生组织p53蛋白阳性率为25.0%(2/8),胃癌为68.4%(13/19),在不典型增生及胃癌组织中,其异倍体的FI值、PI值和p53蛋白阳性率与二倍体者比较,均有显著性差异(P＜0.05).结论胃癌组织p53蛋白的表达水平高于癌前病变及正常胃粘膜组织;随病变向恶性转化,p53蛋白表达水平、PI值及异倍体率均增高.因此,检测p53蛋白表达水平对胃癌的诊断具有一定意义.     

Etoposide, dexamethasone, cytarabine, and cisplatin in vincristine, doxorubicin, and dexamethasone-refractory myeloma

Based on remarkable activity in refractory lymphomas, a combination of etoposide, cisplatin (both administered by 4-day continuous infusions), cytarabine (Ara-C), and dexamethasone (EDAP) was evaluated in 20 patients with advanced myeloma refractory to standard melphalan and prednisone (MP) and/or vincristine, Adriamycin (doxorubicin; Adria Laboratories, Columbus, OH), and dexamethasone (VAD) and even to high doses of melphalan (HDM) (seven patients). Forty percent of patients responded regardless of previously recognized risk factors (eg, duration of drug resistance, tumor mass, and serum lactic dehydrogenase [LDH] level). While the median survival was only 4.5 months, patients with good performance (Zubrod less than 2) and low or intermediate tumor stage survived more than 14 months compared with only 2 months for the remaining group. EDAP could be readily administered in the outpatient clinic, but neutropenic fever prompted hospital admission in 80% of patients, half of whom developed penumonia and sepsis, a fatal outcome in four patients. Severe myelosuppression was of short duration, so that subsequent cycles could be administered every 3 to 4 weeks. No serious extramedullary toxicity, including renal toxicity, was encountered. Marrow toxicity and hence infectious complications may be reduced by elimination of Ara-C without compromising treatment efficacy. We conclude that the lack of cross-resistance with VAD and even HDM makes EDAP or a similar combination an attractive regiment to be formally explored in an alternating sequence with VAD in high-risk myeloma.     

Stress,coping, and hope

Hope is discussed in many literatures and from many perspectives. In this essay hope is discussed from the vantage of psychology and stress and coping theory. Hope and psychological stress share a number of formal properties: both are contextual, meaning‐based, and dynamic, and both affect well‐being in difficult circumstances. Two assumptions underlie this essay: (1) hope is essential for people who are coping with serious and prolonged psychological stress; and (2) hope is not a perpetually self‐renewing resource; it has peaks and valleys and is at times absent altogether. The relationship between hope and coping is dynamic and reciprocal; each in turn supports and is supported by the other. This relationship is illustrated with two adaptive tasks common across situations that threaten physical or psychological well‐being—managing uncertainty and coping with a changing reality. The essay describes ways in which coping fosters hope when it is at low ebb as well as ways in which hope fosters and sustains coping over the long term. Copyright © 2010 John Wiley & Sons, Ltd.     

Myelodysplastic syndromes, aging, and age: correlations, common mechanisms, and clinical implications

Myelodysplastic syndromes (MDS) are a heterogenous group of myeloid neoplasms that develop primarily in elderly patients. Although a specific molecular basis for the predominant incidence of MDS in higher age groups remains unknown, several lines of evidence suggest that the biology of aging and the pathogenesis of MDS share several genetic, epigenetic, and molecular features. The current review attempts to delineate these common aspects as well as additional discriminative features that are specific for MDS and thus help explaining disease-evolution and progression. In addition, the present review discusses age as an important prognostic factor and co-variable to be considered in treatment algorithms in MDS.     

Appendectomy,tonsillectomy, and neoplasia

Reports in the literature that study the frequency of cancer in individuals who have had their tonsils or appendix or both removed are reviewed. Some investigators found a high incidence of solid cancers—in particular, breast and colon neoplasms—in female patients who have had appendectomy, but others disagreed. The association of tonsillectomy and/or appendectomy with the later development of malignant lymphomas is not proven.     

Premenopausal intakes of vitamins A, C, and E, folate, and carotenoids, and risk of breast cancer.

Intakes of vitamins A, C, and E, folate, and carotenoids have been hypothesized to reduce the risk of breast cancer. However, previous epidemiological studies on these nutrients and breast cancer risk have been inconclusive, and have included primarily postmenopausal women. We examined the intake of these nutrients in relation to breast cancer risk among 90,655 premenopausal women ages 26-46 years in 1991 in the Nurses' Health Study II. Nutrient intake was assessed with a validated food-frequency questionnaire at baseline in 1991 and in 1995. During 8 years of follow-up from 1991 to 1999, we documented 714 incident cases of invasive breast cancer. Overall, none of the vitamins and carotenoids was strongly related to a reduced risk of breast cancer. However, intake of vitamin A, including preformed vitamin A and carotenoids, was associated with a reduced risk of breast cancer among smokers; participants in the highest quintile of total vitamin A intake had a multivariate relative risk of 0.28 (95% confidence interval 0.12-0.62; P, test for trend <0.001; P, test for interaction <0.001) compared with those in the lowest quintile of intake. We found no evidence that higher intakes of vitamins C and E, and folate in early adult life reduce risk of breast cancer. However, intake of vitamin A may be related to a reduced risk of breast cancer among smokers.