18FDG-PET-CT improves specificity of preoperative lymph-node staging in patients with intestinal but not diffuse-type esophagogastric adenocarcinoma

Introduction

The accuracy of preoperative lymph-node staging in patients with adenocarcinoma of the esophagogastric junction (AEG) or gastric cancer (GC) is low. The aim of this study was to assess the accuracy of [18F]fluorodeoxyglucose positron emission tomography/computed tomography (PET-CT) for lymph-node staging in patients with AEG or GC, with or without neoadjuvant treatment.

Neuroimaging for Lewy body disease: Is the in vivo molecular imaging of α-synuclein neuropathology required and feasible?

Alpha-synuclein aggregation is a neuropathological hallmark of many neurodegenerative diseases including Parkinson's disease (PD), Parkinson's disease with dementia (PDD) and dementia with Lewy bodies (DLB), collectively termed the α-synucleinopathies. Substantial advances in clinical criteria and neuroimaging technology over the last 20 years have allowed great strides in the detection and differential diagnosis of these disorders. Nevertheless, it is clear that whilst the array of different imaging modalities in clinical use allow for a robust diagnosis of α-synucleinopathy in comparison to healthy subjects, there is no clear diagnostic imaging marker that affords a reliable differential diagnosis between the different forms of Lewy body disease (LBD) or that could facilitate tracking of disease progression. This has led to a call for a biomarker based on the pathological hallmarks of these diseases, namely α-synuclein-positive Lewy bodies (LBs). This potentially may be advantageous in terms of early disease detection, but may also be leveraged into a potential marker of disease progression. We here aim to firstly review the current status of neuroimaging biomarkers in PD and related synucleinopathies. Secondly, we outline the rationale behind α-synuclein imaging as a potential novel biomarker as well as the potential benefits and limitations of this approach. Thirdly, we attempt to illustrate the likely technical hurdles to be overcome to permit successful in vivo imaging of α-synuclein pathology in the diseased brain. Our overriding aim is to provide a framework for discussion of how to address this major unmet clinical need.     

乳腺癌腋窝淋巴结清扫术后阴性淋巴结数目的临床意义(英文)

Objective: The purpose of this study was to evaluate the impact of the negative lymph node (LN) count on the survival of the breast cancer patients in early stage after the axillary dissection. Methods: The breast cancer patients with T1-2N0-1M0 stage between January 2001 and December 2005 in Jiangsu Cancer Hospital, who underwent the axillary LNs dissection, were enrolled in this study. We analyzed the data of these patients including information of follow-up and postoperative pathological results. All patients were divided into two groups according to the axillary LN status and each group was divided into four subgroups according to the negative LN count. Cox regression analysis was performed to screen the pathological factor including the negative LN count on the survival and to compare the different negative LN count on the survival. Results: COX proportional hazard regression model showed that the survival of the breast cancer was significantly associated with the negative LN count. In T1-2N0 group, when the negative LN count was 3 or less, 4 to 5, 6 to 9 and 10 or more, the median survival time was (82.6 ± 4.1) months, (101.5 ± 1.3) months, (104.7 ± 1.0) months, and (110.5 ± 0.9) months respectively (P < 0.05). In T1-2N1 group, when the negative LN count was 6 or less, 7 to 8, 9 to 10 and 11 or more, the median survival time was (95.4 ± 1.9) months, (101.8 ± 1.1) months, (104.9 ± 1.0) months, and (106.5 ± 0.9) months respectively (P < 0.05). Conclusion: The negative LN count can reflect the adequacy of the axillary dissection. Increasing negative LN count is independently associated with improved survival in pT1-2N0M0 or pT1-2N1M0 staging breast cancer patients. The negative LN count should be considered for incorporation into staging for breast cancer with the axillary LN dissection.     

Impaired development and dysfunction of endothelial progenitor cells in type 2 diabetic mice

AimDysfunction of circulating endothelial progenitor cells (EPCs) has been shown to affect the development of microvascular diseases in diabetes patients. The aim of this study was to elucidate the development and mechanical dysfunction of EPCs in type 2 diabetes (T2D).MethodsThe colony-forming capacity of EPCs and differentiation potential of bone marrow (BM) c-Kit(+)/Sca-I(+) lineage-negative mononuclear cells (KSL) were examined in T2D mice, db/db mice and KKA^y mice, using EPC colony-forming assay (EPC-CFA).ResultsT2D mice had fewer BM stem/progenitor cells, and proliferation of KSL was lowest in the BM of db/db mice. In T2D mice, the frequency of large colony-forming units (CFUs) derived from BM-KSL was highly reduced, indicating dysfunction of differentiation into mature EPCs. Only a small number of BM-derived progenitors [CD34(+) KSL cells], which contribute to the supply of EPCs for postnatal neovascularization, was also found. Furthermore, in terms of their plasticity to transdifferentiate into various cell types, BM-KSL exhibited a greater potential to differentiate into granulocyte macrophages (GMs) than into other cell types.ConclusionT2D affected EPC colony formation and differentiation of stem cells to mature EPCs or haematopoietic cells. These data suggest opposing regulatory mechanisms for differentiation into mature EPCs and GMs in T2D mice.     

血清HA、LN、CPⅢ和Ⅳ-C测定在160例肝纤维化患者诊断过程中的应用

目的探讨慢性乙型病毒性肝炎血清透明质酸(HA)、层粘连蛋白(LN)、Ⅲ型前胶原(PCⅢ)和Ⅳ型胶原(Ⅳ-C)在肝纤维化诊断中的应用价值。方法采用放射免疫分析法(R IA)检测160型慢性乙型病毒性患者血清HA、LN、PCⅢ和Ⅳ-C水平,并与肝组织活检纤维化程度进行相关性分析。结果各组慢性乙型病毒性肝炎患者血清HA、LN、PCⅢ和Ⅳ-C水平均高于正常对照组(p<0.05),与肝纤维化活动水平及程度呈密切正相关(p<0.01)。结论血清HA、LN、PCⅢ和Ⅳ-C水平能较好地反映乙型病毒性肝炎的慢性化程度和肝纤维化的活动水平及程度,联合检测可明显提高肝纤维化诊断的准确性和可靠性。     

透明质酸钠对剖宫产产妇血清基质金属蛋白酶9、一氧化氮、层粘蛋白及炎性因子的影响

目的:探讨透明质酸钠对剖宫产产妇血清基质金属蛋白酶9(MMP-9)、一氧化氮(NO)、层粘蛋白(LN)及炎性因子的影响.方法:选取2010年11月～ 2012年10月于该院进行常规处理的45例剖宫产产妇为对照组,并将同一时期采用透明质酸钠处理的45例产妇选为观察组,然后将两组产妇产前与产后不同时间的血清MMP-9、NO、LN及炎性因子水平进行比较.结果:观察组产后不同时间的血清MMP-9高于对照组,NO、LN及炎性因子水平低于对照组,P值均＜0.05,均有统计学差异.结论:透明质酸钠对剖宫产产妇血清MMP-9、NO、LN及炎性因子的影响较为明显,对于控制粘连及感染的发生均有积极的临床作用.     

Tspan8 and CD151 promote metastasis by distinct mechanisms

AimCD151 and Tspan8 are metastasis-promoting tetraspanins. To define whether Tspan8 and CD151 fulfil redundant or additive activities, Tspan8 and CD151 were stably knocked-down in highly metastatic rat pancreatic adenocarcinoma BSp73ASML cells (ASML^wt, ASML-Tspan8^kd, ASML-CD151^kd).ResultsASML-CD151^kd and ASML-Tspan8^kd cells metastasise via the lymphatics to the lung with delay and a 2–3-fold increased survival time compared to ASML^wt cells. Yet, CD151 and Tspan8 distinctly contribute to metastasis. Pronounced adhesion of ASML-Tspan8^kd cells is due to CD151 associating with the alpha3 integrin chain, whereas strikingly increased ASML-CD151^kd cell motility is efficiently inhibited by anti-beta4. These opposing Tspan8 and CD151 activities are due to distinct beta4 recruitment into Tspan8 complexes, accompanied by beta4 phosporylation, src recruitment, focal adhesion kinase (FAK) and Ras activation. On the other hand, CD151 associates more readily with proteases, particularly matrix metalloproteinase (MMP)13 and MMP9, than Tspan8. The stronger CD151–MMP association is accompanied by pronounced collagen I and IV and laminin111 degradation, also seen in metastatic tissue, and strengthens invasiveness.ConclusionCD151 and Tspan8 coordinately promote metastasis, where Tspan8 overrides the adhesive features of CD151 by recruiting integrins out of adhesion into motility promoting complexes. CD151 more efficiently than Tspan8 recruiting and activating MMP9 and MMP13 creates a path for migrating tumour cells.