排序方式: 共有28条查询结果,搜索用时 842 毫秒
1.
2.
Z W Gu F M Li X D Feng S T Voong 《Biomaterials, medical devices, and artificial organs》1983,11(2-3):211-219
Both the homogeneous and heterogeneous hydrolysis of five new acrylic polymers having aspirin-moieties, i.e. polymers of beta-(acetylsalicylyloxy)ethyl methacrylate, beta-(acetylsalicylyloxy) propyl methacrylate,beta-(acetylsalicylyloxy) ethyl acrylate, beta-hydroxy-gamma-(acetylsalicylyloxy) propyl methacrylate, beta-hydroxy-gamma-(acetylsalicylyloxy) propyl acrylate were investigated in acidic or alkaline medium at 30 degrees C or 60 degrees C, respectively. It was observed that the chief hydrolyzed product is always aspirin with minor amount of salicylic acid. 相似文献
3.
Wenji Guo Xuan Hui Salem Alfaifi Lori Anderson Scott Robertson Russell Hales Chen Hu Todd McNutt Stephen Broderick Jarushka Naidoo Richard Battafarano Stephen Yang K. Ranh Voong 《Practical radiation oncology》2018,8(4):e239-e248
Purpose
In patients with non-small cell lung cancer (NSCLC) who undergo trimodality therapy (chemoradiation followed by surgical resection), it is unknown whether limiting preoperative radiation dose to the uninvolved lung reduces postsurgical morbidity. This study evaluated whether radiation fall-off dose parameters to the contralateral lung that is unaffected by NSCLC are associated with postoperative complications in NSCLC patients treated with trimodality therapy.Methods and materials
We retrospectively reviewed NSCLC patients who underwent trimodality therapy between March 2008 and October 2016, with available restored digital radiation plans. Fischer's exact test was used to assess associations between patient and treatment characteristics and the development of treatment-related toxicity. Spearman rank correlation was used to measure the strength of association between dosimetric parameters.Results
Forty-six patients were identified who received trimodality therapy with intensity modulated radiation (median, 59.4 Gy; range, 45-70) and concurrent platinum doublet chemotherapy, followed by surgical resection. The median age was 64.9 years (range, 45.6-81.6). The median follow-up time was 1.9 years (range, 0.3-8.4). Twenty-four (52.2%) patients developed any-grade pulmonary toxicity and 14 (30.4%) patients developed grade 2+ pulmonary toxicity. There was an increased incidence of any-grade pulmonary toxicity in patients with contralateral lung volume receiving at least 20 Gy (V20) ≥7% compared with <7% (90%, n = 9 vs 41.7%, n = 15; P = .01). Similarly, contralateral lung V10 ≥20% was associated with an increased rate of any-grade pulmonary toxicity compared with V10 <20% (80%, n = 12 vs 38.7%, n = 12; P = .01). Pneumonectomy/bilobectomy was associated with grade 2+ pulmonary toxicity (P = .04).Conclusions
Patients who received a higher radiation fall-off dose volume parameter (V20 ≥7% and V10 ≥20%) to the contralateral uninvolved lung had a higher incidence of any-grade postoperative pulmonary toxicity. Limiting radiation fall-off dose to the uninvolved lung may be an important modifiable radiation parameter in limiting postoperative toxicity in trimodality patients. 相似文献4.
Zhang H Cui Y Voong N Sabatino M Stroncek DF Morisot S Civin CI Wayne AS Levine BL Mackall CL 《Journal of immunotherapy (Hagerstown, Md. : 1997)》2011,34(2):187-195
Natural killer (NK) cells can mediate potent antitumor effects, but factors regulating the efficiency of tumor lysis remain unclear. Studies in allogeneic stem cell transplantation highlight an important role for killer cell immunoglobulin-like receptor (KIR) mismatch in overcoming human leukocyte antigen-mediated inhibitory signals. However, other activating and inhibitory signals also modulate tumor lysis by NK cells. We used rhIL15 and artificial antigen presenting cells expressing CD137L and IL15Rα to activate and expand peripheral blood NK cells (CD137L/IL15 NK) up to 1000-fold in 3 weeks. Compared with resting NK cells, CD137L/IL15 NK cells show modest increases in KIR expression and substantial increases in NKG2D, tumor necrosis factor-related apoptosis-inducing ligand, and natural cytotoxicity receptors (NCRs: NKp30, NKp44, NKp46). Compared with resting NK cells, CD137L/IL15 NK cells mediate enhanced cytotoxicity against allogeneic and autologous tumors and KIR signaling did not substantially inhibit cytotoxicity. Rather, tumor lysis by CD137L/IL15 activated NK cells was predominantly driven by NCR signaling as blockade of NCRs dramatically diminished the lysis of a wide array of tumor targets. Furthermore, tumor lysis by CD137L/IL15 NK cells was tightly linked to NCR expression levels that peaked on day 8 to 10 after NK activation, and cytotoxicity diminished on subsequent days as NCR expression declined. We conclude that KIR mismatch is not a prerequisite for tumor killing by CD137L/IL15 NK cells and that NCR expression provides a biomarker for predicting potency of CD137L/IL15 NK cells in studies of NK cell-based immunotherapy. 相似文献
5.
Kim M Liao J Dowling ML Voong KR Parker SE Wang S El-Deiry WS Kao GD 《Cancer research》2008,68(9):3440-3449
Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) has attracted interest as an anticancer treatment, when used in conjunction with standard chemotherapy. We investigated the mechanistic basis for combining low-dose TRAIL with microtubule-targeting agents that invoke the mitotic checkpoint. Treatment of T98G and HCT116 cells with nocodazole alone resulted in a robust mitotic block with initially little cell death; low levels of cell death were also seen with TRAIL alone at 10 ng/mL final concentration. In contrast, the addition of low-dose TRAIL to nocodazole was associated with maximally increased caspase-3, caspase-8, and caspase-9 activation, which efficiently abrogated the mitotic delay and markedly increased cell death. In contrast, the abrogation of mitotic checkpoint and increased cell death were blocked by inhibitors of caspase-8 and caspase-9 or pan-caspase inhibitor. The addition of TRAIL to either nocodazole or paclitaxel (Taxol) reduced levels of the mitotic checkpoint proteins BubR1 and Bub1. BubR1 mutated for the caspase cleavage sites, but not wild-type BubR1, was resistant to cleavage induced by TRAIL added to nocodazole, and partially blocked the checkpoint abrogation. These results suggest that adding a relatively low concentration of TRAIL to antimicrotubule agents markedly increases complete caspase activation. This in turn accentuates degradation of spindle checkpoint proteins such as BubR1 and Bub1, contributes to abrogation of the mitotic checkpoint, and induces cancer cell death. These results suggest that TRAIL may increase the anticancer efficacy of microtubule-targeting drugs. 相似文献
6.
7.
Karen E. Hoffman K. Ranh VoongThomas J. Pugh MD Heath SkinnerLawrence B. Levy MS Vinita TakiarSeungtaek Choi MD Weiliang DuSteven J. Frank MD Jennifer JohnsonJames Kanke CMD Rajat J. KudchadkerAndrew K. Lee MD Usama MahmoodSean E. McGuire MD PhD Deborah A. Kuban MD 《International journal of radiation oncology, biology, physics》2014
8.
Corinne N. Thompson My V. T. Phan Nguyen Van Minh Hoang Pham Van Minh Nguyen Thanh Vinh Cao Thu Thuy Tran Thi Thu Nga Maia A. Rabaa Pham Thanh Duy Tran Thi Ngoc Dung Voong Vinh Phat Tran Vu Thieu Nga Le Thi Phuong Tu Ha Thanh Tuyen Keisuke Yoshihara Claire Jenkins Vu Thuy Duong Hoang Le Phuc Pham Thi Ngoc Tuyet Nguyen Minh Ngoc Ha Vinh Nguyen Tran Chinh Tang Chi Thuong Ha Manh Tuan Tran Tinh Hien James I. Campbell Nguyen Van Vinh Chau Guy Thwaites Stephen Baker 《The American journal of tropical medicine and hygiene》2015,92(5):1045-1052
9.
Understanding the mechanisms leading to transformation of early B-lineage precursors is an important step leading to rational design of new treatments for precursor (pre)-B-cell leukemia. We used normal mouse pre-B cells to determine if and how transforming growth factor (TGF)-beta1 affects these precursors to the B-cell lineage and whether transformed pre-B cells respond to TGF-beta1. We found that normal pre-B cells proliferating in the presence of interleukin (IL)-7 enter cell-cycle arrest after exposure to TGF-beta1. However, clonally related IL-7-independent tumors induced by oncogenes abl + myc or raf + myc have reduced sensitivity to TGF-beta1. In contrast, tumor cells induced by myc alone remain sensitive to TGF-beta1 growth suppression. These results suggest that lesions in different molecular signaling pathways can lead to loss of TGF-beta1 sensitivity in a single cell type. The approach of using normal pre-B-cell lines and transformation by overexpression of different oncogenes provides a system to compare and contrast molecular pathways that lead to full malignancy. 相似文献
10.