TNF-α和低氧对胰腺癌细胞表达VEGF-A、C的调节

目的:探讨细胞活素肿瘤坏死因子-α(TNF-α)、SNAP(S-Nitroso-Nacetyl-penicillamine)对胰腺癌细胞产生血管内皮生长因子A、C(VEGF-A、C)的调节.方法:用Northern杂交和Western杂交法分析6种人胰腺癌细胞株中VEGF-A、C基因和蛋白的表达;以TNF-α或SNAP刺激其中两个细胞株后用逆转录-聚合酶链式反应技术(RT-PCR)分析其VEGF-A、C基因的表达.结果:Northern杂交法显示这6种胰腺癌细胞株均有4.1kb VEGF-A基因和2.4kb VEGF-C基因的表达;Western杂交法显示它们均有分子量为43kD的VEGF-A蛋白质和分子量为55kD的VEGF-C蛋白质的表达.RT-PCR分析法显示:TNF-α使细胞株COLO-357产生VEGF-A、VEGF-C mRNA分别减少约1～2.5倍、1～2倍,使细胞株CAPAN-1产生VEGF-A、VEGF-C mRNA分别减少约1倍、1.6～2.5倍;而SNAP刺激细胞株COLO-357产生VEGF-A mRNA增加约5倍,刺激细胞株CAPAN-1产生VEGF-A mRNA增加约4倍,但对这两种细胞株产生VEGF-C mRNA均无明显刺激作用.结论:细胞活素TNF-α和低氧通过调节血管内皮生长因子A、C的表达而影响胰腺癌细胞的生物学特性,抑制癌细胞的增殖,促进其凋亡、死亡或进展、恶化.     

Human Tumor–infiltrating Lymphocytes Transfected with Tumor Necrosis Factor Gene Could Augment Cytotoxicity to Autologous Tumor Cells

Human tumor–infiltrating lymphocytes (TILs) derived from pleural or ascitic fluid were incubated with recombinant interleukin 2 and transfected with human tumor necrosis factor (TNF) a gene by the lipofection procedure. The resulting TILs secreted significant amounts of TNF in the culture supernatant and exhibited cytotoxicity against established cell lines, such as K562 and Daudi, and autologous tumor cells. The TNF gene–transfected TILs exhibited an augmented killing of autologous tumor cells.     

Regulators of Cardiac Cell Growth, Differentiation, and Apoptosis

The pathogenesis of heart hypertrophy and failure have been the focus of intense clinical and basic science investigation, yet the signal transduction pathways and molecular process that underlie the compensatory growth process that ultimately leads to heart failure remain enigmatic. Since ventricular myocytes have exited the cell cycle, growth of the myocardium in response to hemodynamic load occurs by cellular hypertrophy and not by hyperplasia. In this article, we document the potential involvement of tumor suppressor pocket proteins and cell cycle regulators that may impinge on the growth, differentiation, and apoptosis of cardiac muscle. This revised version was published online in August 2006 with corrections to the Cover Date.     

Effects of tumor necrosis factor alpha on parathyroid hormone-induced increases in osteoblastic cell cyclic AMP

Summary Tumor necrosis factor α (10⁻¹⁰–10⁻⁸M) had no effects on cyclic AMP production by the osteoblastic osteosarcomal cells, Saos-2 and G292, or normal rat calvarial cells. The cytokine did, however, inhibit the parathyroid hormone (PTH)-induced effect on cyclic AMP in the Saos-2 and normal rat osteoblastic cells. This inhibitory effect did not occur on prostaglandin E₂-induced cyclic AMP increases in the osteoblastic cells. Interleukin-1 (10 U/ml −100 U/ml) did not produce any effect on basal levels or PTH-induced cyclic AMP increases in these cells.     

颌骨造釉细胞瘤64例临床分析

本文对我院１９５４－１９９０年收治的６４例颌骨造釉细胞瘤进行了回顾性分析，未发现１例恶性。特别是我们在长期工作实践中发现肿瘤与周围正常骨质有较明显的分界。遂于１９６３年开始试行颌骨内种瘤出术，至１９９０年６月已经成功地施了１２例，１例因手术时肿物巨大而且合并感染于术后１０年复发外，其余１１例术后随访年６个月－２７年，中位１２年１０个月均无复发。发种手术损伤小，方法简单，无损美容，预后性，特别是对颌     

Effect of Glass Transition Temperature on the Stability of Lyophilized Formulations Containing a Chimeric Therapeutic Monoclonal Antibody

Purpose. The purpose of this study is to highlight the importance of knowing the glass transition temperature, T_g, of a lyophilized amorphous solid composed primarily of a sugar and a protein in the interpretation of accelerated stability data. Methods. Glass transition temperatures were measured using DSC and dielectric relaxation spectroscopy. Aggregation of protein in the solid state was monitored using size-exclusion chromatography. Results. Sucrose formulation (T_g ~ 59°C) when stored at 60°C was found to undergo significant aggregation, while the trehalose formulation (T_g ~ 80°C) was stable at 60°C. The instability observed with sucrose formulation at 60°C can be attributed to its T_g (~59°C) being close to the testing temperature. Increase in the protein/sugar ratio was found to increase the T_gs of the formulations containing sucrose or trehalose, but to different degrees. Conclusions. Since the formulations exist in glassy state during their shelf-life, accelerated stability data generated in the glassy state (40°C) is perhaps a better predictor of the relative stability of formulations than the data generated at a higher temperature (60°C) where one formulation is in the glassy state while the other is near or above its T_g.     

急性脑梗塞患者血清肿瘤坏死因子水平变化的观察

采用双抗体夹心ＥＬＩＳＡ法对３０例正常对照和３６例急性脑梗塞患者血清肿瘤坏死因子（ＴＮＦ）水平进行了检测。结果显示：急性脑梗塞组血清ＴＮＦ水平显著高于正常对照组，血清ＴＮＦ水平变化与脑梗塞容积大小密切相关，恢复期血清ＴＮＦ水平显著降低。结果提示，ＴＮＦ参与了脑梗塞发生后病理变化过程，检测血清ＴＮＦ对判定脑梗塞容积大小有一定的临床意义。     

Purification of antigenically intact Ro ribonucleoproteins; biochemical and immunological evidence that the 52-kD protein is not a Ro protein.

Anti-Ro sera immunoprecipitate Ro ribonucleoproteins (RNPs) from human cell extracts. Ro RNPs are biochemically heterogeneous particles whose functions are unknown and whose exact composition remains controversial. In addition to 60-kD Ro and to La proteins, a 52-kD polypeptide (p52) has been proposed to be a stable component of the Ro RNPs. To confirm the immunological studies supporting this hypothesis, we have biochemically purified Ro RNPs from HeLa cells using non-denaturing conditions. Ro RNPs segregated into three distinct populations, one of which only contained hY5 RNA (RohY5 RNPs). No p52 co-purified with Ro RNPs. Despite the absence of p52, purified Ro RNPs had biochemical and immunological properties identical to those of unfractionated Ro RNPs. Many anti-Ro sera only recognize p52 in immunoblots, and are said to be monospecific anti-p52. Preincubation with purified RohY5 RNPs (free of p52) of all human anti-Ro (including so-called monospecific anti-p52) sera abolished their capacity to immunoprecipitate Ro RNPs from unfractionated HeLa cell extracts. Conversely, preincubation of anti-Ro sera with purified p52 protein specifically inhibited recognition of p52 in immunoblots, but did not interfere with immunoprecipitation of Ro RNPs. Our data demonstrate that anti-p52 antibodies do not target intact Ro RNPs, nor do they target the native 60-kD Ro protein. Contrary to previous reports, p52 protein is not a stable component of antigenically intact Ro RNPs.     

Effective segmental chemoembolization of advanced hepatocellular carcinoma with tumor thrombus in the portal vein

Purpose: Evaluate therapeutic results of transcatheter segmental hepatic artery chemo-oily-embolization (segmental TAE) against advanced hepatocellular carcinomas (HCC) accompanied by portal tumor thrombus (PTT). Methods: Segmental TAE was performed in nine patients with hepatic cirrhosis and advanced HCCs accompanied by PTT. Four subsegmental portal branches were obstructed by PTT in three patients, and two were obstructed in the remaining six patients. TAE was performed into the targeted segmental hepatic artery followed by embolization with gelatin sponge particles. Results: In one patient undergoing subsequent resection, a marked anticancer effect on the PTT was demonstrated histologically. In the eight other patients who did not undergo subsequent resection, the cumulative survival rates were 67% at 6 months, 44% at 1 year, and 22% at 2 years. No serious complications were noted. Conclusions: This therapeutic approach is thought to be a useful treatment for HCC with PTT, because it reinforces anticancer effects and can be performed more safely than conventional transcatheter arterial embolization.     

大肠黏膜癌变过程中PTEN和p27的表达及相关性研究

目的 :探讨PTEN及p2 7在大肠黏膜癌变过程中的表达及两者的相关性。方法 :采用免疫组织化学S -P法检测了 5 8例大肠癌 ,15例腺瘤性息肉及 11例配对的癌旁正常组织中抑癌基因PTEN和 p2 7的蛋白表达。分析PTEN和 p2 7的表达情况及与各种临床病理特征的关系及两者的相关性。结果 :在癌旁正常组织、大肠腺瘤性息肉、大肠癌组织中PTEN表达率分别为 (97.3± 4 .3) % ,(85 .2± 16 .8) % ,(13.8± 17.6 ) % ,呈递减趋势。大肠癌DukesA/B期组PTEN蛋白的高表达率为 88.9% ,明显高于DukesC/D期组中的 5 1.6 %。PTEN的高表达率与性别、年龄、肿瘤的大小、部位、分化程度、有无淋巴结转移无关。p2 7主要表达在细胞核 ,也有少量表达在细胞浆。在癌旁正常组织、大肠腺瘤性息肉、大肠癌组织中p2 7高表达率分别为 (98.8± 1.0 8) % ,(86 .0± 13.6 ) % ,(5 6 .8± 2 6 .0 ) % ,呈递减趋势。在大肠癌高、中分化组中 p2 7蛋白的表达率为 71.4 % ,明显高于低分化组中的 2 3.1%。p2 7的高表达率与患者的Dukes分期、性别、年龄、肿瘤的大小、部位及有无淋巴结转移无关。在大肠癌组织中 ,PTEN与 p2 7蛋白的表达呈正相关 (r =0 .6 4 2 )。结论 :PTEN及p2 7表达在癌旁正常组织、大肠腺瘤性息肉、大肠癌组织中均呈递减趋势 ,提示P