Eco\|geographical distribution, biological characters and conservation of \%Brachystachyum \%Keng were studied. The coverage of \%B. densiflorum \%forest increased from 40%~45% to over 90% through rejuvenesced method...Eco\|geographical distribution, biological characters and conservation of \%Brachystachyum \%Keng were studied. The coverage of \%B. densiflorum \%forest increased from 40%~45% to over 90% through rejuvenesced method by conservation \%in situ; \%with the \%ex situ \%strategy, the total individuals of \%B. densiflorum \%var. \%villosum \%increased from 2 to 181 during 5 years (1989~1994), and its mean height reached 3.81 m, its basal\|diameter was 1.95 cm.展开更多
目的:探讨微小分子核糖核酸(miR)-126-3p在甲状腺癌中的表达,探讨其生物学功能。方法:RT-PCR检测35例甲状腺癌、癌旁组织以及三种甲状腺癌细胞系(TPC-1、FTC-133、8505C)中miR-126-3p表达量;将甲状腺癌细胞分为类似物组(mimic)和对照组(...目的:探讨微小分子核糖核酸(miR)-126-3p在甲状腺癌中的表达,探讨其生物学功能。方法:RT-PCR检测35例甲状腺癌、癌旁组织以及三种甲状腺癌细胞系(TPC-1、FTC-133、8505C)中miR-126-3p表达量;将甲状腺癌细胞分为类似物组(mimic)和对照组(NC),分别转染miR-126-3p mimic及阴性对照质粒。两组细胞增殖、凋亡分别采用Brdu-ELISA法和流式细胞术检测,Transwell小室法检测两组细胞迁移和侵袭。结果:35例癌组织中miR-126-3p相对表达量显著低于癌旁组织(0.384±0.028 vs 0.981±0.039,t=10.291,P<0.05);在三种甲状腺癌细胞中,TPC-1细胞中miR-126-3p相对表达量最低;与NC组比较,mimic组甲状腺癌细胞TPC-1增殖受到显著的抑制,第3天两组间开始表现出统计学差异(P<0.05);与NC组比较,mimic组甲状腺癌细胞TPC-1凋亡显著增加[(15.32±3.20)%vs(8.12±1.17)%,t=4.623,P<0.05],迁移受到抑制(26.68±4.48 vs 82.21±3.65,t=17.789,P<0.05),侵袭受到抑制(12.28±1.03 vs 34.43±2.10,t=8.103,P<0.05)。结论:甲状腺癌组织中miR-126-3p表达降低,上调miR-126-3p表达可以显著抑制甲状腺癌细胞增殖、促进凋亡、抑制迁移和侵袭,miR-126-3p可能作为一种抑癌基因在甲状腺癌中发挥重要的生物学功能。展开更多
文摘Eco\|geographical distribution, biological characters and conservation of \%Brachystachyum \%Keng were studied. The coverage of \%B. densiflorum \%forest increased from 40%~45% to over 90% through rejuvenesced method by conservation \%in situ; \%with the \%ex situ \%strategy, the total individuals of \%B. densiflorum \%var. \%villosum \%increased from 2 to 181 during 5 years (1989~1994), and its mean height reached 3.81 m, its basal\|diameter was 1.95 cm.
文摘目的:探讨微小分子核糖核酸(miR)-126-3p在甲状腺癌中的表达,探讨其生物学功能。方法:RT-PCR检测35例甲状腺癌、癌旁组织以及三种甲状腺癌细胞系(TPC-1、FTC-133、8505C)中miR-126-3p表达量;将甲状腺癌细胞分为类似物组(mimic)和对照组(NC),分别转染miR-126-3p mimic及阴性对照质粒。两组细胞增殖、凋亡分别采用Brdu-ELISA法和流式细胞术检测,Transwell小室法检测两组细胞迁移和侵袭。结果:35例癌组织中miR-126-3p相对表达量显著低于癌旁组织(0.384±0.028 vs 0.981±0.039,t=10.291,P<0.05);在三种甲状腺癌细胞中,TPC-1细胞中miR-126-3p相对表达量最低;与NC组比较,mimic组甲状腺癌细胞TPC-1增殖受到显著的抑制,第3天两组间开始表现出统计学差异(P<0.05);与NC组比较,mimic组甲状腺癌细胞TPC-1凋亡显著增加[(15.32±3.20)%vs(8.12±1.17)%,t=4.623,P<0.05],迁移受到抑制(26.68±4.48 vs 82.21±3.65,t=17.789,P<0.05),侵袭受到抑制(12.28±1.03 vs 34.43±2.10,t=8.103,P<0.05)。结论:甲状腺癌组织中miR-126-3p表达降低,上调miR-126-3p表达可以显著抑制甲状腺癌细胞增殖、促进凋亡、抑制迁移和侵袭,miR-126-3p可能作为一种抑癌基因在甲状腺癌中发挥重要的生物学功能。