Objective:To explore the effect and molecular mechanism of SPHK1 in the invasion and metastasis process of non-small-cell lung cancer cells(A549).Methods:Recombinant retrovirus was used to mediate the production of A5...Objective:To explore the effect and molecular mechanism of SPHK1 in the invasion and metastasis process of non-small-cell lung cancer cells(A549).Methods:Recombinant retrovirus was used to mediate the production of A549/vector,A549/SPHK1,A549/scramble,and A549/SPHK1/RNAi that stably expressed or silenced SPHK1.The invasion and migration capacities of A549 cells overexpressing or silencing SPHK1 were determined using Transwell invasion assay and scratch wound repair experiment.The protein and mRNA expression levels of E-cadherin,fibronectin,vimentin in A549/vector,A549/SPHK1,A549/scramble,A549/SPHK1/RNAi were detected with Western blot(WB) and quantitative PCR(QPCR) methods,respectively.Results:Transwell invasion assay and scratch wound repair experiments showed that over-expression of SPHK1 obviously enhanced the invasion and migration capacities of A549 cells.WB and QPCR detection results showed that,the expression of E-cadherin(a molecular marker of epithelial cells) and fibronectin,vimentin(molecular markers of mesenchymal cells) in A549 cells was upregulated after overexpression of SPHK1;while SPHK1 silencing significantly reduced the invasion and metastasis capacities of A549 cells,upregulated the expression of molecular marker of epithelial cells,and downregulated the expression of molecular marker of mesenchymal cells.Conclusions:SPHK1 promotes epithelial mesenchymal transition of non-small-cell lung cancer cells and affects the invasion and metastasis capacities of these cells.展开更多
Traumatic brain injury survivors often experience cognitive deficits and neuropsychiatric symptoms.However,the neurobiological mechanisms underlying specific impairments are not fully understood.Advances in neuroimagi...Traumatic brain injury survivors often experience cognitive deficits and neuropsychiatric symptoms.However,the neurobiological mechanisms underlying specific impairments are not fully understood.Advances in neuroimaging techniques(such as diffusion tensor imaging and functional MRI)have given us new insights on structural and functional connectivity patterns of the human brain in both health and disease.The connectome derived from connectivity maps reflects the entire constellation of distributed brain networks.Using these powerful neuroimaging approaches,changes at the microstructural level can be detected through regional and global properties of neuronal networks.Here we will review recent developments in the study of brain network abnormalities in traumatic brain injury,mainly focusing on structural and functional connectivity.Some connectomic studies have provided interesting insights into the neurological dysfunction that occurs following traumatic brain injury.These techniques could eventually be helpful in developing imaging biomarkers of cognitive and neurobehavioral sequelae,as well as predicting outcome and prognosis.展开更多
Objective To describe the pitfalls in positron emission tomography/computed tomography (PET/CT) imaging and classify them according to the principles of their generation. Methods We summarized retrospectively the ^...Objective To describe the pitfalls in positron emission tomography/computed tomography (PET/CT) imaging and classify them according to the principles of their generation. Methods We summarized retrospectively the ^18F-fluorodeoxyglucose (FDP) PET/CT imaging pitfalls through reviewing the PET/CT images of 872 patients. The pitfalls were divided into artifacts and infrequent physiological uptake, and the artifacts were further classified according to their causes. Meanwhile, we calculated the incidences of various pitfalls. Whether the PET/CT pitfalls influenced the diagnostic decision was analyzed. The appearances of pitfalls in PET were also described. Results Pitfalls could be found in PET/CT images of 684(78.4%) patients. Artifacts were found in 664 (76.15%) patients, and could be classified into self-factor artifacts and equipment-or technology-related artifacts. Among self-factor artifacts, respiratory motion (57.5%), postprandial or hyperglycemia artifacts (2.41%), and metal or high density matter artifacts (1.38%) were frequent. As for equipment-or tectmology-related factors, injection point outleakage or radiotracer contamination (13.88%) and truncation artifacts (1.83%) were most common ones. Infrequent physiological FDG uptakes, including fatty up-take, endometrial uptake, and bilateral breast feeding period uptake, were found in 20 (2.29%) patients. Among all pitfalls, the artifacts in 92 (13.4%) patients and infrequent physiological uptakes in 6 (0.88%) patients affected the diagnostic results. Artifact images in PET could be described as hot or cold area and the images of infrequent physiological uptake were always shown as hot area. Conclusions The incidence of pitfall in PET/CT imaging was high and the causes of pitfalls are various. Among all causes that artifacts generated, respiratory motion is the most common. Some pitfalls may disturb clinical physicians' decision, so it is important to recognize artifacts and physiological uptake, and distinguish them from pathological uptakes.展开更多
基金supported by the Key Projects of Hunan Provincial Edueation Department with the number of 13A103
文摘Objective:To explore the effect and molecular mechanism of SPHK1 in the invasion and metastasis process of non-small-cell lung cancer cells(A549).Methods:Recombinant retrovirus was used to mediate the production of A549/vector,A549/SPHK1,A549/scramble,and A549/SPHK1/RNAi that stably expressed or silenced SPHK1.The invasion and migration capacities of A549 cells overexpressing or silencing SPHK1 were determined using Transwell invasion assay and scratch wound repair experiment.The protein and mRNA expression levels of E-cadherin,fibronectin,vimentin in A549/vector,A549/SPHK1,A549/scramble,A549/SPHK1/RNAi were detected with Western blot(WB) and quantitative PCR(QPCR) methods,respectively.Results:Transwell invasion assay and scratch wound repair experiments showed that over-expression of SPHK1 obviously enhanced the invasion and migration capacities of A549 cells.WB and QPCR detection results showed that,the expression of E-cadherin(a molecular marker of epithelial cells) and fibronectin,vimentin(molecular markers of mesenchymal cells) in A549 cells was upregulated after overexpression of SPHK1;while SPHK1 silencing significantly reduced the invasion and metastasis capacities of A549 cells,upregulated the expression of molecular marker of epithelial cells,and downregulated the expression of molecular marker of mesenchymal cells.Conclusions:SPHK1 promotes epithelial mesenchymal transition of non-small-cell lung cancer cells and affects the invasion and metastasis capacities of these cells.
基金supported by a grant from the Medical Scientific Research Programs of Nanjing Military Command,No.14MS122
文摘Traumatic brain injury survivors often experience cognitive deficits and neuropsychiatric symptoms.However,the neurobiological mechanisms underlying specific impairments are not fully understood.Advances in neuroimaging techniques(such as diffusion tensor imaging and functional MRI)have given us new insights on structural and functional connectivity patterns of the human brain in both health and disease.The connectome derived from connectivity maps reflects the entire constellation of distributed brain networks.Using these powerful neuroimaging approaches,changes at the microstructural level can be detected through regional and global properties of neuronal networks.Here we will review recent developments in the study of brain network abnormalities in traumatic brain injury,mainly focusing on structural and functional connectivity.Some connectomic studies have provided interesting insights into the neurological dysfunction that occurs following traumatic brain injury.These techniques could eventually be helpful in developing imaging biomarkers of cognitive and neurobehavioral sequelae,as well as predicting outcome and prognosis.
文摘Objective To describe the pitfalls in positron emission tomography/computed tomography (PET/CT) imaging and classify them according to the principles of their generation. Methods We summarized retrospectively the ^18F-fluorodeoxyglucose (FDP) PET/CT imaging pitfalls through reviewing the PET/CT images of 872 patients. The pitfalls were divided into artifacts and infrequent physiological uptake, and the artifacts were further classified according to their causes. Meanwhile, we calculated the incidences of various pitfalls. Whether the PET/CT pitfalls influenced the diagnostic decision was analyzed. The appearances of pitfalls in PET were also described. Results Pitfalls could be found in PET/CT images of 684(78.4%) patients. Artifacts were found in 664 (76.15%) patients, and could be classified into self-factor artifacts and equipment-or technology-related artifacts. Among self-factor artifacts, respiratory motion (57.5%), postprandial or hyperglycemia artifacts (2.41%), and metal or high density matter artifacts (1.38%) were frequent. As for equipment-or tectmology-related factors, injection point outleakage or radiotracer contamination (13.88%) and truncation artifacts (1.83%) were most common ones. Infrequent physiological FDG uptakes, including fatty up-take, endometrial uptake, and bilateral breast feeding period uptake, were found in 20 (2.29%) patients. Among all pitfalls, the artifacts in 92 (13.4%) patients and infrequent physiological uptakes in 6 (0.88%) patients affected the diagnostic results. Artifact images in PET could be described as hot or cold area and the images of infrequent physiological uptake were always shown as hot area. Conclusions The incidence of pitfall in PET/CT imaging was high and the causes of pitfalls are various. Among all causes that artifacts generated, respiratory motion is the most common. Some pitfalls may disturb clinical physicians' decision, so it is important to recognize artifacts and physiological uptake, and distinguish them from pathological uptakes.