基于胃癌高发区人群筛查队列的不同胃黏膜病变进展为胃癌风险的前瞻性研究

目的 依托胃癌高发区大规模人群筛查队列分析不同级别胃黏膜病变的患病情况,前瞻性探讨不同胃黏膜病变进展为胃癌的风险,为优化胃癌的筛查策略提供科学依据。方法 基于山东省临朐县胃癌高发区开展的国家上消化道癌早诊早治项目,纳入年龄在40~69岁之间,2012-2018年经内镜筛查和病理诊断明确为各级别胃黏膜病变、且未患有高级别上皮内瘤变（HGIN）或浸润性胃癌的14 087例研究对象,随访至2019年12月31日。随访期内新发胃癌通过重复性胃镜筛查、肿瘤发病和死因登记系统报告以及主动入户随访联合判定,经查阅医院信息管理系统中摘抄的临床病历进行确认。应用Poisson回归模型计算各级别胃黏膜病变进展至胃癌风险的相对危险度（RR）及其95%CI。结果 14 087例研究对象中,胃黏膜正常者仅有8例（0.06%）,最高诊断为浅表性胃炎（SG）、慢性萎缩性胃炎（CAG）、肠上皮化生（IM）和低级别上皮内瘤变（LGIN）分别为7 608例（54.00%）、2 848例（20.22%）、3 103例（22.03%）和520例（3.69%）。经过前瞻性随访,共有109例研究对象诊断为HGIN（63例）和浸润性胃癌（46例）。与基线正常或仅有SG的个体相比,患有CAG、IM和LGIN的个体进展为胃癌的风险依次增加为3.85倍（RR=3.85,95%CI：2.04~7.28）、5.18倍（RR=5.18,95%CI：2.79~9.60）和19.08倍（RR=19.08,95%CI：9.97~36.53）,其中LGIN组进展为HGIN和浸润性胃癌的风险分别为SG/正常组的22.96倍（RR=22.96,95%CI：9.71~54.27）和14.64倍（RR=14.64,95%CI：5.37~39.93）。各个年龄组患有LGIN者随访期间发生胃癌的风险均显著增加。结论 基于胃癌高发区的大样本人群研究显示,绝大多数40~69岁的高发区居民患有不同程度胃黏膜病变。随胃黏膜病变严重程度的增加,随访期间发生胃癌的风险呈级联上升趋势。     

大肠癌及癌前病变的粘液组化研究

应用粘液组化方法AB—PAS、HID—AB、OR—AB、PAT—KOH—PAS、PATB—KOH—PAS显示大肠上皮分泌粘液的类型。结果发现:大肠慢性炎、大肠克隆病及炎性息肉、增生性息肉、幼年性息肉分泌粘液类型与正常粘膜相似(P>0.05),而伴有异型增生的溃疡性结肠炎、管状腺瘤、绒毛状腺瘤、家族性息肉、腺瘤癌变、大肠癌及癌旁粘膜粘液分泌性质与量均有变化。在这些病变中氮乙酰化及含有邻位羟基的氧乙酰化粘液阳性率明显高于正常粘膜(P<0.05)。其检出阳性率与异型增生的程度有关。笔者认为应用粘液组化方法分析大肠癌前病变粘液性质对于判断粘膜上皮恶性倾向提供了有价值的手段。     

立体定向显微手术切除脑内病灶

目的探讨立体定向显微手术切除脑内病灶的可行性。方法应用F.L.FischerZD定向仪,CT定位,对24例脑重要功能区及脑深部病灶进行立体定向开颅显微手术。病变性质胶质瘤14例,脑囊虫2例,转移瘤2例,脑脓肿1例,脑膜瘤1例,动静脉畸形(AVM)1例,海绵状血管瘤1例,异物1例,炎性肉芽肿1例。病灶直径为1.5～3.0cm,＞3.5cm     

颅内病变X-刀治疗效果的CT观察

目的观察颅内病变X-刀治疗后的CT表现,评价疗效.方法51例55个颅内病变X-刀治疗后,直接增强CT扫描.结果病灶消失11例(15个病灶),病灶缩小29例,病灶失增强6例,病灶无变化5例.结论颅内病变X-刀治疗后CT表现能直接反映治疗效果.     

黄参方剂诱导胃癌癌前病变细胞凋亡和影响BCL—2蛋白表达的研究

目的：探讨黄参方剂对胃癌癌前病变细胞凋亡及相关基因表达的影响。方法：将７２例胃癌癌前变患者随机分为２组,治疗组３７例,口服黄参方剂６０ｍｌ／ｄ;对照组３５例,口服维酶素片１２片／天,疗程２月。治疗后胃镜同一部位取材,检测治疗前后细胞凋亡指数和ＢＣＬ－２蛋白的表达。采用原位末端标记法（ＴＵＮＥＬ）检测细胞凋亡,采用免疫组化检测ＢＣＬ－２蛋白的表达。结果：黄参方剂组服药前后细胞凋亡指数分别为（１９．８     

Molecular genetic studies of early breast cancer evolution

Summary In the past few years there has been an explosion in the number of patients diagnosed with hyperplastic breast disease andin situ breast cancer. Based on epidemiological data, these morphologically defined lesions may be categorized as those with little malignant potential (e.g. typical hyperplasia or proliferative disease without atypia [PDWA]), those with significant malignant potential which may already be initiated (e.g. atypical ductal hyperplasia [ADH]), and early transformed lesions which are malignant but not yet invasive (e.g. ductal carcinomain situ [DCIS]). They may represent sequential evolutionary stages in the ontogeny of invasive breast cancer, with each morphologically defined stage resulting from accumulating genetic changes culminating in a transformed clonal lineage capable of invasion and metastasis. Using loss-of-heterozygosity (LOH) analysis, we are studying the genetic changes associated with these lesions in archival tissue samples. 50% (6/12) of the proliferative lesions (PDWA and ADH) and 80% of the DCIS shared their LOH patterns with more advanced lesions from the same breast, strongly supporting a precursor/product relationship between these lesions and the cancers they accompany.     

Post-stroke depression: Relationships with morphological damage and cognition over time

The aim of the present study was to investigate the relationships between poststroke depression (PSD), lesion location and cognitive deficits after stroke. We studied 20 patients within the first month after clinical onset (T1), and one year later (T2). PSD was observed in 55% of patients at T1 and 35% of patients at T2. At T1, depression was reliably correlated with dorsal lesions in the right-hemisphere and anterior lesions in the left hemisphere. Lesion location was no longer a significant factor determining PSD at T2. Changes in PSD, from T1 to T2, were inversely correlated with the performances in cognitive tests exploring the domains of attention, visuospatial learning, executive/motor functions, and with the global composite cognitive score. Our data suggest that: 1) in the mix of influences that may produce PSD, lesion location is the main factor determining mood changes after stroke in the first month; 2) PSD produces deficits in attention, learning, and executive/motor functions, without affecting language and other cognitive domains.

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Sommario Scopo di questo studio sono i rapporti tra la depressione post-stroke (PSD), la localizzazione della lesione cerebrovascolare e i disturbi cognitivi conseguenti alla lesione. Abbiamo studiato 20 pazienti entro il primo mese dall'episodio ictale (T1) ed un anno dopo (T2). La PSD era osservabile nel 55% dei pazienti a T1 e nel 35% dei pazienti a T2. A T1, la PSD era significativamente correlata con lesioni dorsali nell'emisfero di destra e con lesioni anteriori nell'emisfero di sinistra. Queste correlazioni non erano più significative a T2. Le variazioni della PSD da T1 a T2 erano inversamente correlate con le prestazioni dei pazienti a compiti cognitivi di attenzione, apprendimento visuospaziale, funzioni esecutivo/motorie, e con un punteggio cognitivo composito.Questi dati suggeriscono che: 1) tra le numerose cause che possono produrre la PSD, la localizzazione della lesione sembra essere il fattore principale nel primo mese dopo l'episodio cerebrovascolare; 2) la PSD produce disturbi attentivi, di apprendimento visuospaziale ed esecutivi/motori senza determinare disturbi nella sfera del linguaggio e di altre funzioni cognitive.

     

Pentoxifylline and intravenous gamma globulin combination therapy for acute Kawasaki disease

We compared the efficacy of oral administration of pentoxifylline (PTX) and intravenous infusions of gamma globulin (IVGG) combination therapy with that of IVGG in reducing the frequency of coronary-artery lesions (CAL) in children with Kawasaki disease (KD), in a randomized trial. All patients with KD received acetylsalicylic acid (30 mg/kg per day), until the 30th day, after the onset of fever, followed by daily acetylsalicylic acid at a dose of 3-5 mg/kg per day there-after, and intravenous IVGG, 200 mg/kg per day, for 5 consecutive days. In addition, patients randomly assigned to PTX and IVGG combination therapy groups received oral PTX at a dosage of 10 mg/kg per day (low-dose) or 20 mg/kg per day (high-dose), in three divided doses until the 30th day. Patients with KD were all free from CAL prior to treatment. We assessed the presence of CAL by two-dimensional echocardiography which was also done prior to treatment and then twice a week after hospital admission. We detected CAL in 3 of 18 patients (16.7%) in the IVGG therapy group, as compared with 2 of 18 patients (11.1%) in the low-dose PTX and IVGG combination therapy group. There were no significant differences between the two groups. In the next study, we detected CAL in 3 of 21 patients (14.3%) in the IVGG therapy group, as compared with none of 22 patients (0%) in the high-dose PTX and IVGG combination therapy group (² = 6.4, P < 0.02). No adverse side-effects were observed in 79 patients with KD.     

Growth and development in thalassaemia major patients with severe bone lesions due to desferrioxamine

Nine transfusion-dependent -thalassaemia major patients (seven males and two females), aged 4–15 years, with growth retardation and severe rickets-like radiological lesions due to continuous subcutaneous chelation therapy with desferrioxamine (45–75 mg/kg body weight, 6–7 times/week), were seen in our centre during the last 8 years. Serum ferritin levels ranged from 976 to 4115 g/l. There was a progressive decline in growth velocity in these patients 2–3 years before the appearance of rickets-like radiological lesions. All patients underwent surgery to correct genu valgum and/or slipped capital epiphyses. The final height was below the 3rd percentile in six patients (SDS: from –2.9 to –5.2). The short stature was mainly due to a disproportion between upper and lower segments. Six of the patients had an associated sensorineural hearing loss.Conclusion Our data emphasize the importance of an accurate surveillance of the toxic effects of desferrioxamine treatment and warn of the risk of overtreating patients with low iron overload and also suggest a possible individual idiosyncrasy to the adverse effects of chelation therapy.     

An immunohistochemical study of the breast using antibodies to basal and luminal keratins,alpha-smooth muscle actin,vimentin, collagen IV and laminin

Summary The distribution of simple epithelial (K8/18/ 19) and basal (myoepithelial) (K5/14) keratins, -smooth-muscle actin, vimentin, collagen IV and laminin in normal mammary glands and in benign proliferative lesions was studied using monoclonal antibodies (mAbs). These antibodies (Abs) identified myoepithelial cells and luminal cells specifically. In lesions with adenosis and papillomas, the two-layered formation resembled that of normal glands with a purely myoepithelial-epithelial differentiation. In scleradenotic lesions, the main cell was of myoepithelial immunophenotype with intermixed trabecular-tubular proliferations of simple-type epithelium. The sclerosis seems to be the result of an irregular basal lamina synthesis by the myoepithelial cells. In contrast to these lesions, epitheliosis represents a purely intraluminal cell proliferation of clearly simple epithelial immunophenotype and of cells with a basal keratin phenotype, lacking myoepithelial differentiation antigen actin. The basal keratin type epithelium may represent post-stem or intermediate cells developing into luminal epithelium. Epitheliosis appears to be a purely epithelial hyperplasia with striking similarity to the regeneration of normal breast epithelium. The different proliferative patterns may give an explanation for differences in potential cancer risks of patients with these lesions.Dedicated to Prof. Dr. G. Seifert on the occasion of his 70th birthday