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1 than sulfonated dithiaporphyrin 30, HPPH, or Photofrin.
2 of HSP-70 for all photosensitizers including Photofrin.
3 ficantly lower for bacteriochlorins than for Photofrin.
6 Our results showed almost similar uptake of photofrin after 24 h in different glioblastoma cells, bu
9 after DMXAA plus low-dose PDT (1.5 mg.kg(-1) Photofrin) appeared to be dependent on TNF-alpha because
10 ) of 694 nm light was comparable to PDT with Photofrin at 2.5 mg (4 micromol)/kg and 135 J cm(-2) of
14 lts indicated that the anti-tumor effects of photofrin based PDT was strongly augmented by miR-99a ov
15 the molecular mechanisms how the efficacy of photofrin based photodynamic therapy (PDT) was enhanced
16 tosensitization conditions with a porphyrin (Photofrin)-based sensitizer failed to induce a cellular
17 gated the activity of DMXAA as a modifier of Photofrin-based PDT of implanted murine RIF-1 tumors.
19 following an affinity of the photosensitizer Photofrin for collagen-containing vascular basement memb
20 mouse feet after low-dose PDT (1.5 mg.kg(-1) Photofrin); however, there was some enhancement of norma
22 pared with controls such as the FDA-approved Photofrin (LD(50) approximately 10 microM) and clinicall
23 ndard clinical treatment conditions (1 mg/kg Photofrin, light at 630 nm and 150 mW/cm2), which are hi
24 nce in response to systemically administered Photofrin, measured noninvasively using an in vivo fluor
26 the present study, we evaluated the role of Photofrin-mediated PDT in eliciting expression of matrix
27 ble BA mouse mammary carcinoma, we show that Photofrin-mediated PDT induced expression of the hypoxia
28 nduced fibrosarcoma tumors were treated with Photofrin-mediated PDT to a total dose of 135 J/cm(2), d
33 in 2, sulfonated thiaporphyrin 30, HPPH, and Photofrin were also evaluated against Colo-26 cells in c
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