Purpose: When hypertonic solution 20% mannitol solution was injected into vein, inflammatory mediators and Mitogen-activated protein kinases activated by mannitol can directly induce the fading of vascular endothelial...Purpose: When hypertonic solution 20% mannitol solution was injected into vein, inflammatory mediators and Mitogen-activated protein kinases activated by mannitol can directly induce the fading of vascular endothelial cell, which leads to phlebitis. The study aims to observe the influences of reparil-gel N coated at the proximal parts of the puncture point and basing on this along with infusing heated mannitol to veins to the injure and ultrastructure of veins which were infused the 20% mannitol solution by indwelling needle in vein. Methodology: There are 15 adult New Zealand rabbits. We randomly divided 24 ear veins of 12 adult New Zealand rabbits into Control group, Gelatum group, Gel heated group and injected 20% mannitol solution by vein detained needle in three groups. In Gelatum group, we coated the proximal end of the puncture point with a thin layer of compound aescine gel. Based on Gelatum group, we heated 20% mannitol solution to 35oC-37oC in Gel heated group. Then we observed the intravenous parts and took the veins of each group out to observe their morphology and ultrastructural after the second day of transfusion. 6 ear veins of the rest 3 rabbits as Health group weren’t given any interventions, the veins were taken out to observe their morphology. Results: Comparison between Gelatum group and Gelatum heated group on vascular dilatation, Infiltration of inflammatory cell and Formation of thrombus had no significance, P> 0.05, while the case was different for the comparison on injury of vascular wall, perivascular edema and perivascular hemorrhage, P< 0.05). The statistical significance exists between control group and Gelatum group and Gel heated group, P< 0.05. It was observed under the electron microscope that, in control group, the membrane of endothelial cell peeled off and the mitochondria swelled and vacuolized. In Gelatum group, the membrane of endothelial cell was defective, the parts of the mitochondria were fuzzy, intercellular substance was slightly edematous. In Gel heated group, the 展开更多
Emerging evidence suggests that intron-detaining transcripts(IDTs)are a nucleus-detained and polyadenylated mRNA pool for cell to quickly and effectively respond to environmental stimuli and stress.However,the underly...Emerging evidence suggests that intron-detaining transcripts(IDTs)are a nucleus-detained and polyadenylated mRNA pool for cell to quickly and effectively respond to environmental stimuli and stress.However,the underlying mechanisms of detained intron(DI)splicing are still largely unknown.Here,we suggest that post-transcriptional DI splicing is paused at the Bact state,an active spliceosome but not catalytically primed,which depends on Smad Nuclear Interacting Protein 1(SNIP1)and RNPS1(a serine-rich RNA binding protein)interaction.RNPS1 and Bact components preferentially dock at DIs and the RNPS1 docking is sufficient to trigger spliceosome pausing.Haploinsufficiency of Snip1 attenuates neurodegeneration and globally rescues IDT accumulation caused by a previously reported mutant U2 snRNA,a basal spliceosomal component.Snip1 conditional knockout in the cerebellum decreases DI splicing efficiency and causes neurodegeneration.Therefore,we suggest that SNIP1 and RNPS1 form a molecular brake to promote spliceosome pausing,and that its misregulation contributes to neurodegeneration.展开更多
文摘Purpose: When hypertonic solution 20% mannitol solution was injected into vein, inflammatory mediators and Mitogen-activated protein kinases activated by mannitol can directly induce the fading of vascular endothelial cell, which leads to phlebitis. The study aims to observe the influences of reparil-gel N coated at the proximal parts of the puncture point and basing on this along with infusing heated mannitol to veins to the injure and ultrastructure of veins which were infused the 20% mannitol solution by indwelling needle in vein. Methodology: There are 15 adult New Zealand rabbits. We randomly divided 24 ear veins of 12 adult New Zealand rabbits into Control group, Gelatum group, Gel heated group and injected 20% mannitol solution by vein detained needle in three groups. In Gelatum group, we coated the proximal end of the puncture point with a thin layer of compound aescine gel. Based on Gelatum group, we heated 20% mannitol solution to 35oC-37oC in Gel heated group. Then we observed the intravenous parts and took the veins of each group out to observe their morphology and ultrastructural after the second day of transfusion. 6 ear veins of the rest 3 rabbits as Health group weren’t given any interventions, the veins were taken out to observe their morphology. Results: Comparison between Gelatum group and Gelatum heated group on vascular dilatation, Infiltration of inflammatory cell and Formation of thrombus had no significance, P> 0.05, while the case was different for the comparison on injury of vascular wall, perivascular edema and perivascular hemorrhage, P< 0.05). The statistical significance exists between control group and Gelatum group and Gel heated group, P< 0.05. It was observed under the electron microscope that, in control group, the membrane of endothelial cell peeled off and the mitochondria swelled and vacuolized. In Gelatum group, the membrane of endothelial cell was defective, the parts of the mitochondria were fuzzy, intercellular substance was slightly edematous. In Gel heated group, the
基金the Tsinghua-Peking Joint Center for Life Sciences,the Thousand-Talent Young Investigator Program,the IDG/McGovern Institute for Brain Research,the National Natural Science Foundation of China(81371361,92049114,31571097,82101495)The Beijing Municipal Science&Technology Commission(Z181100001518001,Z161100000216154)+1 种基金National Key R&D Program(2017YFC0110205)the Institute for Guo Qiang,Tsinghua University。
文摘Emerging evidence suggests that intron-detaining transcripts(IDTs)are a nucleus-detained and polyadenylated mRNA pool for cell to quickly and effectively respond to environmental stimuli and stress.However,the underlying mechanisms of detained intron(DI)splicing are still largely unknown.Here,we suggest that post-transcriptional DI splicing is paused at the Bact state,an active spliceosome but not catalytically primed,which depends on Smad Nuclear Interacting Protein 1(SNIP1)and RNPS1(a serine-rich RNA binding protein)interaction.RNPS1 and Bact components preferentially dock at DIs and the RNPS1 docking is sufficient to trigger spliceosome pausing.Haploinsufficiency of Snip1 attenuates neurodegeneration and globally rescues IDT accumulation caused by a previously reported mutant U2 snRNA,a basal spliceosomal component.Snip1 conditional knockout in the cerebellum decreases DI splicing efficiency and causes neurodegeneration.Therefore,we suggest that SNIP1 and RNPS1 form a molecular brake to promote spliceosome pausing,and that its misregulation contributes to neurodegeneration.
