19718.10是什么星座_百度知道
19718.10是什么星座
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, February 2003, Pages 185–197
Regular articleA multivariate, spatiotemporal analysis of electromagnetic time-frequency data of recognition memory, , , , , , , , , a Department of Neurology II, Otto von Guericke University, Leipziger Strasse 44, Magdeburg 39120, Germanyb Rotman Research Institute, Baycrest Centre, 3560 Bathurst Street, Toronto, Ontario, M6A 2E1 CanadaElectromagnetic indices of &fast& (above 12 Hz) oscillating brain activity are much more likely to be considerably attenuated by time-averaging across multiple trials than &slow& (below 12 Hz) oscillating brain activity. To the extent that both types of oscillations represent the activity of temporally and topographically separable neural populations, time averaging can cause a loss of brain activity information that is important both conceptually and for multimodal integration with hemodynamic techniques. To address this issue for recognition memory, simultaneous electroencephalography (EEG) and whole-head magnetoencephalography (MEG) recordings of explicit word recognition from 11 healthy subjects were analyzed in two different ways. First, the time course of neural oscillations ranging from theta (4.5 Hz) to gamma (42 Hz) frequencies were identified using single-trial continuous wavelet transforms. Second, traditional analyses of amplitude variations of time-averaged EEG and MEG signals, event-related potentials (ERPs), and fields (ERFs) were performed and submitted to distributed source analyses. To identify data patterns that covaried with the difference between correctly recognized studied (old) words and correctly rejected nonstudied (new) words, a multivariate statistical tool, partial least squares (PLS), was applied to both types of analyses. The results show that ERPs and ERFs are mainly displaying those neural indices of recognition memory that oscillate in the theta (4.5&7.5 Hz), alpha (8&11.5), and to some extent in the beta1 (12&19.5 Hz) frequency range. The sources of the ERPs/ERFs were in good agreement with the topography of theta/alpha/beta 1 oscillations in being confined to the anterior temporal lobe at 400 ms and being distributed across temporal, parietal, and occipital areas between 500 and 700 ms. Gamma oscillations covaried either positively or negatively with theta/alpha/beta1 oscillations. A positive covariance, for instance, was detected over left anterior temporal sensors as early as 200&350 ms and is compatible with studies in rodents showing that gamma and theta oscillations emerge together out of the interaction of the hippocampus and the entorhinal and perirhinal cortices. Fast beta oscillations (20&29.5 Hz), on the other hand, did not strongly covary with slow oscillations and were likely to arise from neural populations not adequately represented in ERPs/ERFs. In summary, by providing a more comprehensive description of electromagnetic signals, time-frequency data are of potential benefit for integrating electrophysiological and hemodynamic indices of brain activity and also for integrating human and animal electrophysiology.KeywordsRecognition; Oscillations; Wavelets; ERPs; MEG; Source analysis; Partial least squares; PLS; N400; LPC
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Correlation of MAGE-A tumor antigens and the efficacy of various chemotherapeutic agents in head and neck carcinoma cellsS. HartmannDepartment of Oral and Maxillofacial Plastic SurgeryUniversity Hospital WürzburgU. KriegebaumDepartment of Oral and Maxillofacial Plastic SurgeryUniversity Hospital WürzburgN. KüchlerDepartment of Oral and Maxillofacial Plastic SurgeryUniversity Hospital WürzburgR. C. BrandsDepartment of Oral and Maxillofacial Plastic SurgeryUniversity Hospital WürzburgC. LinzDepartment of Oral and Maxillofacial Plastic SurgeryUniversity Hospital WürzburgA. C. KüblerDepartment of Oral and Maxillofacial Plastic SurgeryUniversity Hospital WürzburgU. D. A. Müller-RichterDepartment of Oral and Maxillofacial Plastic SurgeryUniversity Hospital WürzburgOriginal ArticleDOI:
10.-013-0936-0Cite this article as: Hartmann, S., Kriegebaum, U., Küchler, N. et al. Clin Oral Invest (9. doi:10.-013-0936-0
The present study examined the relationship between MAGE-A tumor antigens and the efficacy of diamindichloridoplatin (DDP), 5-fluorouracil (5-FU), docetaxel, and paclitaxel for in vitro treatment of head and neck cancer.
In the present study, five cell lines of human squamous cell carcinomas were treated with DDP (25–400 μM), 5-FU (0.75–12 mM), docetaxel (1.56–25 nM), and paclitaxel (1.56–25 nM) for a period of 24 or 48 h. The efficacy of the agents was observed dynamically using real-time cell analysis. Subsequently, the expression levels of MAGE-A1, MAGE-A5, MAGE-A8, MAGE-A9, MAGE-A11, and MAGE-A12 were determined by quantitative real-time polymerase chain reaction. Chemosensitivity and MAGE-A-expression were correlated by linear regression.
The tumor cell lines showed a highly differentiated response to the chemotherapeutic agents. Expression of MAGE-A11 was significantly associated with a poorer response to treatment with DDP, 5-FU, docetaxel, and paclitaxel. Two cell lines, one of which was MAGE-A11-positive, showed a significant and concentration-dependent cisplatin-induced growth spurt during the first 24 h after treatment. MAGE-A5 was connected to a positive effect on treatment with paclitaxel within the first 24 h after application. In association with docetaxel treatment, MAGE-A8 was connected to a poorer susceptibility.
The results describe, for the first time, a correlation between these MAGE-A tumor antigens and the susceptibility of head and neck cancer cells to DDP, 5-FU, docetaxel, and paclitaxel.
These findings could affect the antineoplastic treatment of patients with MAGE-A11-positive tumors.
1.van der Bruggen P et al (1991) A gene encoding an antigen recognized by cytolytic T lymphocytes on a human melanoma. Science 254(–16472.De Plaen E et al (1994) Structure, chromosomal localization, and expression of 12 genes of the MAGE family. Immunogenetics 40(5):360–3693.Chomez P et al (2001) An overview of the MAGE gene family with the identification of all human members of the family. Cancer Res 61(14):4.Barker PA, Salehi A (2002) The MAGE proteins: emerging roles in cell cycle progression, apoptosis, and neurogenetic disease. J Neurosci Res 67(6):705–7125.Muller-Richter UD et al (2008) Different expression of MAGE-A-antigens in foetal and adult keratinocyte cell lines. Oral Oncol 44(7):628–6336.Yang B et al (2007) MAGE-A, mMage-b, and MAGE-C proteins form complexes with KAP1 and suppress p53-dependent apoptosis in MAGE-positive cell lines. Cancer Res 67(20):7.Lian Y et al (2012) Expressions of MAGE-A10 and MAGE-A11 in breast cancers and their prognostic significance: a retrospective clinical study. J Cancer Res Clin Oncol 138(3):519–5278.Qiu G, Fang J, He Y (2006) 5′ CpG island methylation analysis identifies the MAGE-A1 and MAGE-A3 genes as potential markers of HCC. Clin Biochem 39(3):259–2669.Muller-Richter UD et al (2010) MAGE-A antigens in patients with primary oral squamous cell carcinoma. Clin Oral Investig 14(3):291–29610.Hussein YM et al (2011) The melanoma-associated antigen-A3, -A4 genes: relation to the risk and clinicopathological parameters in breast cancer patients. Mol Cell Biochem 351(1–2):261–26811.Nardiello T et al (2011) MAGE-A inhibits apoptosis in proliferating myeloma cells through repression of Bax and maintenance of survivin. Clin Cancer Res 17(13):12.Ries J et al (2005) Investigation of the expression of melanoma antigen-encoding genes (MAGE-A1 to -A6) in oral squamous cell carcinomas to determine potential targets for gene-based cancer immunotherapy. Int J Oncol 26(3):817–82413.Krauss E et al (2011) MAGE-A antigens in lesions of the oral mucosa. Clin Oral Investig 15(3):315–32014.Mollaoglu N et al (2011) Prediction of recurrence using exfoliative cytology and melanoma-associated antigen-A mRNA analysis following wide excision of oral squamous cell carcinoma: short report. Cytopathology 22(6):387–39115.Muller-Richter UDA et al (2010) Impact of MAGE-A antigens on taxane response in oral squamous cell carcinoma. Oncol Lett 1(1):181–18516.Heo DS et al (1989) Biology, cytogenetics, and sensitivity to immunological effector cells of new head and neck squamous cell carcinoma lines. Cancer Res 49(18):17.Muller-Richter UD et al (2009) Analysis of expression profiles of MAGE-A antigens in oral squamous cell carcinoma cell lines. Head Face Med 5:1018.Dowejko A et al (2012) The human HECA interacts with cyclins and CDKs to antagonize Wnt-mediated proliferation and chemoresistance of head and neck cancer cells. Exp Cell Res 318(5):489–49919.Dowejko A et al (2009) The human homolog of the Drosophila headcase protein slows down cell division of head and neck cancer cells. Carcinogenesis 30(10):20.Arias LR, Perry CA, Yang L (2010) Real-time electrical impedance detection of cellular activities of oral cancer cells. Biosens Bioelectron 25(10):21.Stiewe T (2007) The p53 family in differentiation and tumorigenesis. Nat Rev Cancer 7(3):165–16822.Monte M et al (2006) MAGE-A tumor antigens target p53 transactivation function through histone deacetylase recruitment and confer resistance to chemotherapeutic agents. Proc Natl Acad Sci U S A 103(30):123.Doyle JM et al (2010) MAGE-RING protein complexes comprise a family of E3 ubiquitin ligases. Mol Cell 39(6):963–97424.Feldman DR et al (2008) Medical treatment of advanced testicular cancer. JAMA 299(6):672–68425.Liu W et al (2008) The melanoma-associated antigen A3 mediates fibronectin-controlled cancer progression and metastasis. Cancer Res 68(19):26.Perera FP (1996) Molecular epidemiology: insights into cancer susceptibility, risk assessment, and prevention. J Natl Cancer Inst 88(8):496–50927.Wilson EM (2010) Androgen receptor molecular biology and potential targets in prostate cancer. Ther Adv Urol 2(3):105–11728.Tsai JR et al (2007) Differential expression profile of MAGE family in non-small-cell lung cancer. Lung Cancer 56(2):185–19229.Camisasca DR et al (2011) Oral squamous cell carcinoma: clinicopathological features in patients with and without recurrence. ORL J Otorhinolaryngol Relat Spec 73(3):170–17630.Simpson AJ et al (2005) Cancer/testis antigens, gametogenesis and cancer. Nat Rev Cancer 5(8):615–625
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