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排序方式: 共有801条查询结果,搜索用时 812 毫秒
731.
The findings presented in this discussion seek to make a contribution to quality of life (QOL) research, by highlighting the import of factors affecting the communication of primary stage head and neck cancer patient's experiences of suffering after treatments by their clinicians. Qualitative research methodology based on open-ended interviews with 18 survivors of American Joint Committee on Cancer (AJCC) Stage I and Stage II, squamous cell carcinoma of the head and neck (SCCHN) were used. The interviews were transcribed verbatim and thematically analysed. In this preliminary analysis, three important themes emerged: (1) a self diminished by cancer; (2) the fear of addiction to pain medications; and (3) hopelessness and the loss of meaning in life after SCCHN. Our present findings indicate that SCCHN patients understand their experiences of cancer and under-report their experiences of suffering mainly because of fear. These include fears of: being further diminished by SCCHN, fears of addiction, and an inability to cope with the additional losses associated with SCCHN. As a consequence, and perhaps, because of a failure the part of clinicians and patients to adequately address these fears, SCCHN patients may also experience greater psychological morbidity, becoming fatalistic about biomedicine's ability to restore them to health after cancer, or related symptoms, including pain, despite being 'cured.' This study provides a perspective on why this under-reporting occurs, thereby potentially enhancing clinician-patient communication and the QOL of SCCHN patients who present with curable disease. 相似文献
732.
Sun SY Zhou Z Wang R Fu H Khuri FR 《Cancer biology & therapy》2004,3(11):1092-8; discussion 1099-1101
Farnesyltransferase inhibitors (FTIs) have been demonstrated to induce growth arrest or apoptosis independent of Ras mutation. Alternatively, Akt has been proposed as a potential target for the FTI's actions. This study investigated whether Lonafarnib was effective in inhibiting the growth of human nonsmall cell lung cancer (NSCLC) cells and elucidated the role of Akt in mediating such growth inhibitory effects. Lonafarnib, at clinical achievable concentration ranges, was effective in inhibiting the growth of 10 NSCLC cell lines, particularly after a prolonged treatment, regardless of Ras mutational status. Lonafarnib arrested cells growth at G(1) or G(2)/M phase in the majority tested cell lines. However it induced apoptosis when cells were cultured in a low serum (0.1%) medium. The majority of NSCLC cell lines expressed undetectable level of phosphorylated Akt (p-Akt). Lonafarnib at up to 10 muM did not decrease either total Akt level or p-Akt level in any of the tested cell lines, even after a 48 h treatment. Unexpectedly, Lonafarnib even increased p-Akt level in one cell line, although it was as sensitive as others to Lonafarnib treatment and underwent G(2)/M arrest. Bovine serum albumin completely rescued cells from Lonafarnib-induced apoptosis in low serum medium, indicating that proteins rather than cytokines or growth factors in serum masks Lonafarnib's pro-apoptotic effect. Therefore, we conclude that Lonafarnib is effective in inhibiting the growth of NSCLC cells either via growth arrest or induction of apoptosis without downregulation of Akt. 相似文献
733.
Death receptor (DR) 4 or 5, on binding to its ligand, tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), triggers apoptosis via activating the caspase-8-mediated caspase cascade. Certain anticancer drugs up-regulate the expression of these receptors and thereby induce apoptosis or enhance TRAIL-induced apoptosis. In this study, we explored the ability of methyl-2-cyano-3,12-dioxooleana-1,9-dien-28-oate (CDDO-Me) to activate the extrinsic DR-mediated apoptotic pathway in human lung cancer cells. We found that CDDO-Me not only activated caspase-8 but also induced expression of DRs, particularly DR5, in a p53-independent mechanism. Correspondingly, CDDO-Me augmented TRAIL-induced apoptosis in these cells regardless of p53 status as evidenced by enhanced DNA fragmentation and activation of caspase cascades, suggesting that CDDO-Me-induced DRs are functionally active. Moreover, silencing of DR5 expression using small interfering RNA suppressed apoptosis induced by CDDO-Me alone or by combination of CDDO-Me and TRAIL, indicating that DR5 up-regulation is required for induction of apoptosis by CDDO-Me and for enhancement of TRAIL-induced apoptosis by CDDO-Me. CDDO-Me rapidly activated c-Jun NH(2)-terminal kinase (JNK) before DR up-regulation and caspase-8 activation. Moreover, application of the JNK-specific inhibitor SP600125 blocked CDDO-Me-induced increases in JNK activation, DR up-regulation, caspase-8 activation, and DNA fragmentation. These results show that activation of JNK pathway results in CDDO-Me-induced DR up-regulation, caspase-8 activation, and apoptosis. Collectively, we conclude that CDDO-Me induces apoptosis via the JNK-mediated DR up-regulation in human lung cancer cells. 相似文献
734.
735.
目的;建立泽兰合剂质量控制方法。方法:采用TLC对金银花,红花进行定性鉴别,HPLC测定绿原酸的含量。结果:TLC鉴别方法专属性强。含量测定绿原酸在0.2-1.0μg间有良好的线性关系。回收率为98.67%,RSD为2.19%。结论:本法简便,准确,重现性好,可作为该制剂的质量控制方法。 相似文献
736.
737.
Immunochemical studies on the differential binding properties of two monoclonal antibodies reacting with Tn red cells 总被引:2,自引:0,他引:2
Two monoclonal antibodies (MoAbs), BRIC 66 (IgM) and BRIC 111 (IgG1), were produced by immunizing mice with ovarian cyst blood group A1 glycoprotein and Tn red cells (RBCs), respectively. Their specificities were determined by inhibitions using Tn sialoglycoproteins (SGPs), mucins (armadillo [ASG] and ovine [OSG] submaxillary glycoproteins), and monosaccharides. BRIC 66 agglutinated both Tn and group A RBCs and reacted immunohistochemically with both the vascular endothelium and tumor cells from a group A adenocarcinoma, BRIC 66 was inhibited by N-acetylgalactosamine (GalNAc), Tn SGPs, and mucins on both hemagglutination inhibition tests and radioimmunoassay. BRIC 111 agglutinated Tn RBCs only, and it specifically stained tumor cells from a group O patient's breast carcinoma and a group A patient's adenocarcinoma. In hemagglutination inhibition tests, BRIC 111 was readily inhibited by Tn SGPs, only partially inhibited by GalNAc, and not inhibited by mucins. In a sensitive radioimmunoassay, BRIC 111 was inhibitable by GalNAc. Tn SGP was 2000-fold more effective as an inhibitor than the mucins (ASG and desialized OSG), which contain a high content of terminal alpha-GalNAc-O-serine (threonine) residues. It is postulated that BRIC 66 is specific for terminal alpha-GalNAc units in carbohydrate chains. The exclusive reaction of BRIC 111 with Tn SGP indicates a combining site larger than GalNAc alpha-1, which probably includes amino acid residues in juxtaposition to GalNAc in Tn SGP. In view of its specific agglutination of Tn RBCs, BRIC 111 is a useful reagent for the examination of polyagglutinable RBCs. 相似文献
738.
R. N. Khuri S. K. Agulian D. A. Aklanjian 《Pflügers Archiv : European journal of physiology》1973,345(3):265-270
Summary A method is presented for the construction, calibration and utilization of a single unit ion-selective microelectrode of the internal capillary configuration. The microelectrode is ideally suited for in situ applications. The microelectrode capacity can be made as small as 10 nanoliters. It is superior to previously constructed microelectrode cells in that it combines the ion-selective and the reference electrodes into one physical unit. 相似文献
739.
740.