Risk of Neoplastic Change in Ileal Pouches in Familial Adenomatous Polyposis

Introduction

Neoplastic change in ileal reservoirs after proctocolectomy has been reported in patients with familial adenomatous polyposis. We aim to determine the incidence and progression of neoplastic change in the ileal pouch of familial adenomatous polyposis patients at our institution.

Methods

A retrospective review of all patients who underwent proctocolectomy for familial adenomatous polyposis with construction of an ileal pouch from 1972 to 2007 was performed. Data and status at follow-up were retrieved from the Mayo Clinic Colorectal Surgery Pouch database.

Results

One hundred seventeen patients were identified with a median age of 26, 52 were male. Ileal reservoirs included J-pouch (a?=?104), Kock pouch (n?=?9), S-pouch (n?=?3), and W-pouch (n?=?1). Median follow-up was 125 months. Polyps were biopsied in 33 patients: non-dysplastic polyps (n?=?2), low-grade dysplasia (n?=?30), and adenocarcinoma (n?=?1). No patients had high-grade dysplasia. Median time to development of dysplasia was 149 months. Adenocarcinoma developed in one patient after 284 months. Risk of dysplasia at 10, 20, and 25 years was 17, 45, and 69 %, respectively.

Conclusion

Though there is a high incidence of low-grade dysplasia in the ileal reservoir in familial adenomatous polyposis patients, high-grade dysplasia and cancer occur rarely. Patients with low-grade dysplasia may still necessitate regular follow-up.     

A genetic variant of NLRP1 gene is associated with asbestos body burden in patients with malignant pleural mesothelioma

The presence of asbestos bodies (ABs) in lung parenchyma is considered a histopathologic hallmark of past exposure to asbestos fibers, of which there was a population of longer fibers. The mechanisms underlying AB formation are complex, involving inflammatory responses and iron (Fe) metabolism. Thus, the responsiveness to AB formation is variable, with some individuals appearing to be poor AB formers. The aim of this study was to disclose the possible role of genetic variants of genes encoding inflammasome and iron metabolism proteins in the ability to form ABs in a population of 81 individuals from North East Italy, who died after having developed malignant pleural mesothelioma (MPM). This study included 86 genetic variants distributed in 10 genes involved in Fe metabolism and 7 genetic variants in two genes encoding for inflammasome molecules. Genotypes/haplotypes were compared according to the number of lung ABs. Data showed that the NLRP1 rs12150220 missense variant (H155L) was significantly correlated with numbers of ABs in MPM patients. Specifically, a low number of ABs was detected in individuals carrying the NLRP1 rs12150220 A/T genotype. Our findings suggest that the NLRP1 inflammasome might contribute in the development of lung ABs. It is postulated that the NLRP1 missense variant may be considered as one of the possible host genetic factors contributing to individual variability in coating efficiency, which needs to be taken when assessing occupational exposure to asbestos.     

bcl-1 REARRANGEMENT AND CYCLIN D1 PROTEIN EXPRESSION IN MANTLE CELL LYMPHOMA

Centrocytic lymphoma, or mantle cell lymphoma (MCL), is characterized by a chromosomal translocation t(11;14) (q13;q32) involving the bcl-1 locus on chromosome 11. Cyclin D1 is a cell-cycle regulatory protein essential for G1–S transition and has been identified as a potential transforming gene affected by the translocation. In this study, 32 cases of MCL were analysed for the bcl-1 rearrangement and cyclin D1 protein expression. In 17 cases, a rearrangement at the major translocation cluster of bcl-1 could be detected. Twenty-four cases exhibited nuclear cyclin D1 expression that was not detectable in other B-cell lymphomas ( n =40) or in normal B-cells. In nine MCL samples, cyclin D1 was expressed without a detectable bcl-1 rearrangement. The detection of a t(11;14) by means of classical cytogenetics in one of these cases, however, may suggest that this discrepancy could be due to chromosomal breakages outside the typical translocation cluster region. In two cases, a bcl-1 rearrangement was not accompanied by cyclin D1 expression. This study provides further evidence that cyclin D1 is involved in the pathogenesis of MCL and can be exploited as a diagnostic marker in the differential diagnosis of B-cell lymphomas and in the identification of MCL.     

脂多糖诱导体外培养骨骼肌卫星细胞表达肝细胞生长因子的变化

目的:研究证实,在众多生长因子中,肝细胞生长因子无论在体外还是体内都可以激活静止状态的肌卫星细胞,修复受损肌肉。采用脂多糖刺激体外培养的骨骼肌卫星细胞,观察肌卫星细胞产生肝细胞生长因子以及肌卫星细胞增殖分化的变化。方法:实验于2006-07/2007-05在华中科技大学同济医学院同济医院创伤外科实验室完成。①实验材料:健康SD成年雄性大鼠,体质量150～200g,由华中科技大学同济医学院实验动物中心提供。实验过程中对动物处置符合实验动物伦理学标准。②实验方法:分离SD大鼠后肢部分股四头肌肉进行骨骼肌卫星细胞的培养。取第2代细胞爬片,待细胞增殖到80%密度时,丙酮固定细胞,常规处理后进行α-sarcometricactin细胞免疫化学染色鉴定,以成纤维细胞作为阴性对照。取第3代骨骼肌卫星细胞,应用0,5,10,20mg/L脂多糖刺激体外培养的大鼠骨骼肌卫星细胞,采用ELISA方法测细胞培养液中的肝细胞生长因子的浓度。取第4代骨骼肌卫星细胞,用含体积分数为0.10胎牛血清的培养基配制成单个细胞悬液,调整浓度为5×107L-1,分成两组,一组加入10mg/L脂多糖,另一组不加任何干预。采用噻唑蓝(MTT)法测定卫星细胞的增殖率。结果:①以未经脂多糖处理的无血清培养基培养的肌肉卫星细胞培养液为对照,将对照组和5,10,20mg/L脂多糖处理组比较,各实验组肝细胞生长因子浓度明显高于对照组(P<0.05)。②5,10,20mg/L脂多糖刺激骨骼肌卫星细胞分泌的肝细胞生长因子水平差异无显著性。③肝细胞生长因子在脂多糖刺激后36h分泌浓度最高。④脂多糖刺激肌卫星细胞的增殖分化明显高于未经刺激的肌卫星细胞。结论:①脂多糖可诱导骨骼肌卫星细胞自分泌肝细胞生长因子。②不同质量浓度脂多糖培养基中肝细胞生长因子水平差异无统计学意义。③脂多糖具有促进骨骼肌卫星细胞增殖分化的效应。     

"Strukturierter Fragebogen Simulierter Symptome"

The current article addresses the psychometric qualities of the German version of the Structured Inventory of Malingered Symptomatology (SIMS), a self-report measure of malingering. The SIMS was administered to a heterogeneous sample of forensic patients (n=62) and undergraduate students (n=204). Within the student sample, some undergraduates were instructed to feign certain pathological conditions, while others were asked to respond honestly to the SIMS items. The findings indicate that the German version of the SIMS demonstrates adequate test-retest stability and internal consistency. In the patient sample, the SIMS was found to correlate strongly with manipulative and antisocial personality features. More specifically, SIMS scores were higher in sexually delinquent patients with antisocial personality disorders. Our findings support the SIMS as a valuable screening tool for malingering of psychiatric symptoms.