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- Suzuki, F., et al.
(författare)
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Tumor-specificity and type of cell death induced by phenoxazines
- 2007
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Ingår i: Anticancer Research. - 0250-7005 .- 1791-7530. ; 27:6B, s. 4233-4238
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Tidskriftsartikel (refereegranskat)abstract
- Phenoxazines have shown diverse biological activities, but tumor-specific cytotoxic activity has not been investigated. A total of 24 phenoxazine derivatives (WM1-24) was investigated for their relative cytotoxicity against human tumor cell lines vs. normal cells. WM7 and WM8 showed the highest tumor-specificity index of 4.3 and 4.8, respectively. Considerable difference in drug-sensitivity was found among these tumor cell lines. Human promyelocytic leukemia HL-60 cells showed the highest sensitivity to both WM7 and WM8, followed by human oral squamous cell carcinoma (HSC-2, HSC-3, HSC-4), and human gingival fibroblast (HGF), pulp cell (HPC) and periodontal ligament fibroblast (HPLF) were the most resistant. WM7 and WM8 induced little or no internucleosomal DNA fragmentation, and activated caspase-3 in HSC-2, HSC-4 and human glioblastoma T98G cells. These compounds failed to induce autophagic cell death, as judged by acridine orange and microtubule-associated protein I light chain 3 (LC3)-GFP assays. These results suggested that the higher cytotoxicity of WM7 and WM8 are derived from the positively-charged quaternary nitrogen substituents on the phenoxazine ring and the electron density of nitrogen at N12, and that inhibition of autophagy is not always coupled with apoplosis induction.
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| 3. |
- Dunham, Christine M., et al.
(författare)
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Structures of tRNAs with an expanded anticodon loop in the decoding center of the 30S ribosomal subunit
- 2007
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Ingår i: RNA. - : Cold Spring Harbor Laboratory. - 1355-8382 .- 1469-9001. ; 13:6, s. 817-823
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Tidskriftsartikel (refereegranskat)abstract
- During translation, some +1 frameshift mRNA sites are decoded by frameshift suppressor tRNAs that contain an extra base in their anticodon loops. Similarly engineered tRNAs have been used to insert nonnatural amino acids into proteins. Here, we report crystal structures of two anticodon stem–loops (ASLs) from tRNAs known to facilitate +1 frameshifting bound to the 30S ribosomal subunit with their cognate mRNAs. ASLCCCG and ASLACCC (5'–3' nomenclature) form unpredicted anticodon–codon interactions where the anticodon base 34 at the wobble position contacts either the fourth codon base or the third and fourth codon bases. In addition, we report the structure of ASLACGA bound to the 30S ribosomal subunit with its cognate mRNA. The tRNA containing this ASL was previously shown to be unable to facilitate +1 frameshifting in competition with normal tRNAs (Hohsaka et al. 2001), and interestingly, it displays a normal anticodon–codon interaction. These structures show that the expanded anticodon loop of +1 frameshift promoting tRNAs are flexible enough to adopt conformations that allow three bases of the anticodon to span four bases of the mRNA. Therefore it appears that normal triplet pairing is not an absolute constraint of the decoding center.
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| 7. |
- Tsuboi, M, et al.
(författare)
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Mortality and mobility after hip fracture in Japan: a ten-year follow-up.
- 2007
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Ingår i: Journal of Bone and Joint Surgery: British Volume. - 2044-5377. ; 89:4, s. 461-466
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Tidskriftsartikel (refereegranskat)abstract
- We studied prospectively the change over ten years in mortality, walking ability and place of residence after a hip fracture in 753 patients in Japan. We compared the deaths observed in these patients with those expected in the general population, matched for age, gender and calender year at the time of fracture. The survival rate decreased dramatically for two years after the event and the mortality risk remained higher for ten years. This risk was approximately double that of the general population, even at ten years after fracture. The risk was higher, and remained so for longer, in younger rather than in older patients. The proportion of patients who were able to walk outdoors alone, with or without an assistive device, was 68% (514) before fracture. This decreased to 56% (340) by one year after and remained stable at approximately 63% (125) until ten years. The proportion of patients living in their own home was 84% (629) before fracture, 81% (491) one year later, and then remained stable at approximately 86% (171) until ten years after the event.
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