ras和nm23的表达与胃癌转移的相关性研究

目的:观察nm23与ras在原发性胃癌中的表达水平与胃癌淋巴结转移的关系.方法:免疫组化和RT-PCR.结果:通过对80例原发性胃癌的研究表明nm23低表达者淋巴结转移率(90%)比nm23正常表达者高(40%,P<0.05).同时发现p21 ras阳性为65%,p21 ras阳性者淋巴结转移率高于p21 ras阴性者淋巴结转移率(78.5%对57.1%,p<0.05).肿瘤组织如同时具有nm23低表达和ras过表达则有更高的淋巴结转移率(94.12%),而nm23高表达和ras低表达者则淋巴结转移率更低(25%),ras-mRNA半定量分析说明ras的表达与淋巴结转移正相关,结论:nm23低表达和ras过表达在原发性胃癌淋巴结转移中起重要的联合作用.它们可以作为判断胃癌预后的一个生物学标志.     

How to determine post-RCHOP therapy for risk-tailored adult patients with diffuse large B-cell lymphoma,addition of maintenance rituximab or observation: multicenter experience

Background  

In international prognostic index (IPI) risk-tailored adult patients with diffuse large B-cell lymphoma (DLBCL), it is still unclear whether the addition of maintenance rituximab (MR) improves progression-free (PFS) and overall survival (OS), after RCHOP (rituximab, cyclophosphamide, doxorubicin, vincristine and prednisone) therapy.     

Quantitative assessment of left ventricular systolic function in patients with coronary heart disease by velocity vector imaging

Objective: To assess the left ventricular (LV) longitudinal systolic function and asynchrony in patients with coronary atherosclerotic heart disease (CAD) by syngo velocity vector imaging (VVI). Methods: Twenty‐eight control subjects and 79 patients with CAD were examined, including 28 patients with myocardial infarction, 26 patients with coronary lumen stenosis <50%, and 25 patients with myocardial ischemia. According to the results of coronary arteriography and electrocardiogram (ECG), the myocardial segments of the LV of CAD patients were divided into four groups: ischemic, infarcted, nonischemic, and normal. Dynamic imaging was performed on all subjects. The systolic peak strain (Smax), systolic strain rate (SRmax), time to peak strain (PTs), and time to peak strain rate (PTsr) in every cardiac cycle were measured. Results: A total of 1,253 out of 1,712 (96.5%) segments were successfully analyzed with VVI. Smax and SRmax of the ischemic and infarcted segments were impaired in CAD patients. Optimal sensitivity and specificity were obtained with strain and strain rate cutoffs of ?14.08% and ?0.83 s^?1, respectively, for detecting ischemic segments and ?6.65% and ?0.38 s^?1, respectively, for detecting infarcted segments. The PTs and PTsr were significantly longer in the ischemic and infarcted segments compared to those of the control group. Conclusions: Utilizing VVI, the longitudinal strain, strain rate, and peak time in CAD patients are easy to obtain and reproducible. Strain and strain rate cutoff values of abnormal myocardium are valuable for detecting ischemia and infarction. The PTs and PTsr values possibly estimate myocardium asynchrony in CAD patients. (Echocardiography 2012;29:340‐345)     

Roles of Kupffer cells in liver transplantation

Kupffer cells, the resident macrophages of the liver, not only exert phagocytosis but also excrete proinflammatory cytokines. Large amounts of cytokines, produced by activated Kupffer cells, can induce aggravate liver ischemia/reperfusion (I/R) injury. Also, Kupffer cells that express protective genes protect from I/R injury after liver transplantation. Due to their key location, Kupffer cells might function as antigen-presenting cells and participate in transplantation immunity. They also seem to play a key role in innate immune responses and host defence through the expression and secretion of soluble inflammatory mediators. With this review we want to assist in improving the understanding of the contribution of Kupffer cells in liver I/R injury and the development of the transplantation immune. We hope that the delineation of the complex mechanisms of dysregulation may inspire the design and development of novel treatment approaches.     

Critical role of CD4 T cells in maintaining lymphoid tissue structure for immune cell homeostasis and reconstitution

Loss of the fibroblastic reticular cell (FRC) network in lymphoid tissues during HIV-1 infection has been shown to impair the survival of naive T cells and limit immune reconstitution after antiretroviral therapy. What causes this FRC loss is unknown. Because FRC loss correlates with loss of both naive CD4 and CD8 T-cell subsets and decreased lymphotoxin-β, a key factor for maintenance of FRC network, we hypothesized that loss of naive T cells is responsible for loss of the FRC network. To test this hypothesis, we assessed the consequences of antibody-mediated depletion of CD4 and CD8 T cells in rhesus macaques and sooty mangabeys. We found that only CD4 T-cell depletion resulted in FRC loss in both species and that this loss was caused by decreased lymphotoxin-β mainly produced by the CD4 T cells. We further found the same dependence of the FRC network on CD4 T cells in HIV-1-infected patients before and after antiretroviral therapy and in other immunodeficiency conditions, such as CD4 depletion in cancer patients induced by chemotherapy and irradiation. CD4 T cells thus play a central role in the maintenance of lymphoid tissue structure necessary for their own homeostasis and reconstitution.     

CCR1 blockade reduces tumor burden and osteolysis in vivo in a mouse model of myeloma bone disease

The chemokine CCL3/MIP-1α is a risk factor in the outcome of multiple myeloma (MM), particularly in the development of osteolytic bone disease. This chemokine, highly overexpressed by MM cells, can signal mainly through 2 receptors, CCR1 and CCR5, only 1 of which (CCR1) is responsive to CCL3 in human and mouse osteoclast precursors. CCR1 activation leads to the formation of osteolytic lesions and facilitates tumor growth. Here we show that formation of mature osteoclasts is blocked by the highly potent and selective CCR1 antagonist CCX721, an analog of the clinical compound CCX354. We also show that doses of CCX721 selected to completely inhibit CCR1 produce a profound decrease in tumor burden and osteolytic damage in the murine 5TGM1 model of MM bone disease. Similar effects were observed when the antagonist was used prophylactically or therapeutically, with comparable efficacy to that of zoledronic acid. 5TGM1 cells were shown to express minimal levels of CCR1 while secreting high levels of CCL3, suggesting that the therapeutic effects of CCX721 result from CCR1 inhibition on non-MM cells, most likely osteoclasts and osteoclast precursors. These results provide a strong rationale for further development of CCR1 antagonists for the treatment of MM and associated osteolytic bone disease.