Purpose: The aim of this study was to determine the incidence and pattern of injuries resulting from auto-tricycle crashes among patients in a tertiary referral centre in Ghana. Methods: Data were retrospectively extr...Purpose: The aim of this study was to determine the incidence and pattern of injuries resulting from auto-tricycle crashes among patients in a tertiary referral centre in Ghana. Methods: Data were retrospectively extracted from hospital records of patients who got involved in auto-tricycle crashes and presented to the Accident and Emergency Centre of the Komfo Anokye Teaching Hospital (KATH), over a one-year period using a structured questionnaire. The gathered data were then entered into an electronic database and then analysed with SPSS version 20.0. Results: The incidence of injury following auto-tricycle crashes over the one-year period was 5.9% (95% CI: 4.9% - 7.0%) with a case fatality rate (FR) of 3.8% (95% CI: 1.3% - 8.7%). All the mortalities resulted from head and neck injuries and none of the patients involved wore a crash helmet. Only 5% of those studied wore crash helmets and were all drivers. Closed fractures accounted for 58% of the injuries, followed by open fractures, 28%. The most commonly fractured bones were the tibia/fibula, followed by the femur and then radius/ulna. The most common mechanism of injury was auto-tricycle toppling over (29%). Passengers were the most injured (48%), followed by drivers (37%) and pedestrians (15%). Most (72%) injuries among participants involved a single body part. On the injury severity scale, most (61%) of patients had minor trauma and 38% had major trauma. Conclusion: Auto-tricycle crashes account for 5.9% of injuries at the study site with a case fatality rate of 3.8%. Passengers had a higher injury rate (48%) than drivers (37%). Fractures of the tibia/fibula were most commonly associated with auto-tricycle crashes. Injuries to the head and neck were responsible for the deaths in the study participants and non-use of a crash helmet was associated with mortalities.展开更多
Background Runt-related transcription factor 1 （Runxl） plays a crucial role in hematogenesis and its dysfunction may contribute to leukemogenesis. However, it is not clear whether or not abnormal expression of Runxl...Background Runt-related transcription factor 1 （Runxl） plays a crucial role in hematogenesis and its dysfunction may contribute to leukemogenesis. However, it is not clear whether or not abnormal expression of Runxl will induce leukemia and how the change of Runxl expression level could affect BCR-ABL-induced leukemogenesis. In the present study, we aimed to analyze if abnormal expression of Runxl in BaF3 cells alone would induce teukemogenesis. And we also wanted to know if abnormal expression of Runxl in leukemic cells would affect leukemogenesis. Furthermore, we investigated whether overexpression or knock-down of Runxl in BaF3 cells would induce leukemogenesis. Methods Plasmids containing full-length Runxl cDNA were transduced into BaF3 cells and BaF3-P185wt cells （BCR-ABL transformed BaF3 cells） by electroporation. Plasmids containing a short hairpin RNA of Runxl were transduced into BaF3 cells and BaF3-P185wt cells by electroporation. Runxl expression level was quantified by Western blotting and quantitative real-time PCR. The effects of overexpression or knock-down of Runxl on proliferation, apoptosis and migration of cells were detected in vitro. Then, using MSCV-P185wt-EGFP as a control, we transplanted MSCV-P185wt-Runx1 cells or MSCV-P185wt-shRNA cells into Balb/c mice through tail vein and observed tumorgenesis of the different phenotypes. Results In vitro analysis revealed that overexpression of Runxl in P185wt cells could inhibit cell proliferation and slow down cell migration; while knock-down of Runxl could promote cell proliferation and speed up cell migration. In vivo analysis indicated that mice transplanted with MSCV-P185wt-Runx1 survived longer than controls. In contrast, mice transplanted with MSCV-P185wt-shRNA survived shorter than the control group. Gross pathological analysis revealed that the MSCV-P185wt-Runx1 group had less severe splenomegaly and hepatomegaly compared to the control group, and the MSCV-P185wt-shRNA group had more severe splenomegaly and hepatomegaly. No splenomegaly or hepatomegaly was detected in mice transplanted with MSCV-BaF3-Runxl cells or MSCV-BaF3-shRNA cells. Both the mice of MSCV-BaF3-Runxl group and MSCV-BaF3-shRNA group were healthy with no sign of leukemia for up to three months. Conclusions Overexpression or knock-down of Runxl gene in BaF3 cells alone could not induce leukemogenesis. However, in BaF3-P185wt cells, alteration of Runxl expression could affect BCR-ABL-induced proliferation and migration in vitro and leukemoaenesis in vivo.展开更多
PDRG1(p53 and DNA-damage regulated 1)是实验室通过文库筛选发现的参与NF-kB信号通路调控的一个新基因。已知PDRG1在多种肿瘤中高表达,并参与p53信号通路;同时该基因受UV以及基因毒性等刺激调控。但其在NF-κB信号通路中作用尚未见报...PDRG1(p53 and DNA-damage regulated 1)是实验室通过文库筛选发现的参与NF-kB信号通路调控的一个新基因。已知PDRG1在多种肿瘤中高表达,并参与p53信号通路;同时该基因受UV以及基因毒性等刺激调控。但其在NF-κB信号通路中作用尚未见报道,为了深入研究PDRG1对NF-κB信号通路的调控机理,构建了稳定干涉PDRG1的HeLa细胞系。选择了基于慢病毒载体pLKO.1的感染体系,该慢病毒体系可以同时感染分裂期与非分裂期的细胞,将目的基因干涉序列稳定整合至靶细胞基因组中;再经过抗生素压力筛选后在短时间内获得稳定干涉目的基因表达的细胞株。设计合成PDRG1干涉序列并克隆至pLKO.1载体,转染病毒包装细胞293TN后收集慢病毒上清感染HeLa细胞系,进一步经过嘌呤霉素压力筛选成功获得稳定表达PDRG1干涉序列的细胞株。该稳定细胞株的建立为PDRG1的功能研究提供了必要的实验工具。展开更多
文摘Purpose: The aim of this study was to determine the incidence and pattern of injuries resulting from auto-tricycle crashes among patients in a tertiary referral centre in Ghana. Methods: Data were retrospectively extracted from hospital records of patients who got involved in auto-tricycle crashes and presented to the Accident and Emergency Centre of the Komfo Anokye Teaching Hospital (KATH), over a one-year period using a structured questionnaire. The gathered data were then entered into an electronic database and then analysed with SPSS version 20.0. Results: The incidence of injury following auto-tricycle crashes over the one-year period was 5.9% (95% CI: 4.9% - 7.0%) with a case fatality rate (FR) of 3.8% (95% CI: 1.3% - 8.7%). All the mortalities resulted from head and neck injuries and none of the patients involved wore a crash helmet. Only 5% of those studied wore crash helmets and were all drivers. Closed fractures accounted for 58% of the injuries, followed by open fractures, 28%. The most commonly fractured bones were the tibia/fibula, followed by the femur and then radius/ulna. The most common mechanism of injury was auto-tricycle toppling over (29%). Passengers were the most injured (48%), followed by drivers (37%) and pedestrians (15%). Most (72%) injuries among participants involved a single body part. On the injury severity scale, most (61%) of patients had minor trauma and 38% had major trauma. Conclusion: Auto-tricycle crashes account for 5.9% of injuries at the study site with a case fatality rate of 3.8%. Passengers had a higher injury rate (48%) than drivers (37%). Fractures of the tibia/fibula were most commonly associated with auto-tricycle crashes. Injuries to the head and neck were responsible for the deaths in the study participants and non-use of a crash helmet was associated with mortalities.
文摘Background Runt-related transcription factor 1 （Runxl） plays a crucial role in hematogenesis and its dysfunction may contribute to leukemogenesis. However, it is not clear whether or not abnormal expression of Runxl will induce leukemia and how the change of Runxl expression level could affect BCR-ABL-induced leukemogenesis. In the present study, we aimed to analyze if abnormal expression of Runxl in BaF3 cells alone would induce teukemogenesis. And we also wanted to know if abnormal expression of Runxl in leukemic cells would affect leukemogenesis. Furthermore, we investigated whether overexpression or knock-down of Runxl in BaF3 cells would induce leukemogenesis. Methods Plasmids containing full-length Runxl cDNA were transduced into BaF3 cells and BaF3-P185wt cells （BCR-ABL transformed BaF3 cells） by electroporation. Plasmids containing a short hairpin RNA of Runxl were transduced into BaF3 cells and BaF3-P185wt cells by electroporation. Runxl expression level was quantified by Western blotting and quantitative real-time PCR. The effects of overexpression or knock-down of Runxl on proliferation, apoptosis and migration of cells were detected in vitro. Then, using MSCV-P185wt-EGFP as a control, we transplanted MSCV-P185wt-Runx1 cells or MSCV-P185wt-shRNA cells into Balb/c mice through tail vein and observed tumorgenesis of the different phenotypes. Results In vitro analysis revealed that overexpression of Runxl in P185wt cells could inhibit cell proliferation and slow down cell migration; while knock-down of Runxl could promote cell proliferation and speed up cell migration. In vivo analysis indicated that mice transplanted with MSCV-P185wt-Runx1 survived longer than controls. In contrast, mice transplanted with MSCV-P185wt-shRNA survived shorter than the control group. Gross pathological analysis revealed that the MSCV-P185wt-Runx1 group had less severe splenomegaly and hepatomegaly compared to the control group, and the MSCV-P185wt-shRNA group had more severe splenomegaly and hepatomegaly. No splenomegaly or hepatomegaly was detected in mice transplanted with MSCV-BaF3-Runxl cells or MSCV-BaF3-shRNA cells. Both the mice of MSCV-BaF3-Runxl group and MSCV-BaF3-shRNA group were healthy with no sign of leukemia for up to three months. Conclusions Overexpression or knock-down of Runxl gene in BaF3 cells alone could not induce leukemogenesis. However, in BaF3-P185wt cells, alteration of Runxl expression could affect BCR-ABL-induced proliferation and migration in vitro and leukemoaenesis in vivo.
文摘PDRG1(p53 and DNA-damage regulated 1)是实验室通过文库筛选发现的参与NF-kB信号通路调控的一个新基因。已知PDRG1在多种肿瘤中高表达,并参与p53信号通路;同时该基因受UV以及基因毒性等刺激调控。但其在NF-κB信号通路中作用尚未见报道,为了深入研究PDRG1对NF-κB信号通路的调控机理,构建了稳定干涉PDRG1的HeLa细胞系。选择了基于慢病毒载体pLKO.1的感染体系,该慢病毒体系可以同时感染分裂期与非分裂期的细胞,将目的基因干涉序列稳定整合至靶细胞基因组中;再经过抗生素压力筛选后在短时间内获得稳定干涉目的基因表达的细胞株。设计合成PDRG1干涉序列并克隆至pLKO.1载体,转染病毒包装细胞293TN后收集慢病毒上清感染HeLa细胞系,进一步经过嘌呤霉素压力筛选成功获得稳定表达PDRG1干涉序列的细胞株。该稳定细胞株的建立为PDRG1的功能研究提供了必要的实验工具。
