Background: Attractor-based kinematic gait analysis using the Fatigue Index Kliniken Schmieder (FKS), have been suggested as a sensitive tool to determine motor fatigability in persons with Multiple Sclerosis (pwMS). ...Background: Attractor-based kinematic gait analysis using the Fatigue Index Kliniken Schmieder (FKS), have been suggested as a sensitive tool to determine motor fatigability in persons with Multiple Sclerosis (pwMS). Hypothesis: Depression does not affect the FKS to a similar degree as in pwMS. Methods: We recruited 32 patients with major depression. Data were collected with two accelerometers attached to both ankles. Data were recorded for one minute at the beginning and at the end of the treadmill test. Attractor attributes were used to analyze the data. Results: The mean Fatigue Index Kliniken Schmieder (FKS) was 2.1. The change of the attractor (δM) was 3.7 and the change of variability (δD) was 0.6. Mean values were clearly below values of pwMS with fatigability from a previous publication. However, the individual level values from six individuals—five of them showed pain related comorbidity besides depression—fell within the lower pathological range. There was no correlation between Hamilton depression scale and the attractor attributes (δM and δD). Discussion: Depression does not affect gait as motor fatigability does in pwMS. Results from subjects with pain during the treadmill test show a moderately increased variability and moderately altered attractors.展开更多
Mutations leading to constitutive activation of the Wnt pathway and its target genes are frequently observed in cancer. The Wnt pathway promotes cell proliferation and increasing evidence supports its role also in can...Mutations leading to constitutive activation of the Wnt pathway and its target genes are frequently observed in cancer. The Wnt pathway promotes cell proliferation and increasing evidence supports its role also in cancer cell metabolism. This study aims to elucidate the role of the Wnt/β-catenin target gene CCND1 in these processes in colorectal cancer. We analyzed whether knock-down of CCND1 affects cell cycle progression and energy metabolism in a colorectal cancer cell line. Down-regulation of CCND1 led to retardation of the cell cycle. The proportion of cells in the G0 phase increased, while the amount of cells in the S- and G2/M phase decreased. Interestingly, knock-down of CCND1 changed the perinuclear localization of mitochondria into a homogeneous distribution within the cytosol. In addition CCND1 knock-down led to an increase of the intracellular ATP level indicating that cyclin D1 reduced mitochondrial activity. Our findings suggest that in addition to its role in cell cycle regulation, the Wnt target gene CCND1 regulates mitochondrial localization and inhibits mitochondrial activity in colorectal cancer cells.展开更多
文摘Background: Attractor-based kinematic gait analysis using the Fatigue Index Kliniken Schmieder (FKS), have been suggested as a sensitive tool to determine motor fatigability in persons with Multiple Sclerosis (pwMS). Hypothesis: Depression does not affect the FKS to a similar degree as in pwMS. Methods: We recruited 32 patients with major depression. Data were collected with two accelerometers attached to both ankles. Data were recorded for one minute at the beginning and at the end of the treadmill test. Attractor attributes were used to analyze the data. Results: The mean Fatigue Index Kliniken Schmieder (FKS) was 2.1. The change of the attractor (δM) was 3.7 and the change of variability (δD) was 0.6. Mean values were clearly below values of pwMS with fatigability from a previous publication. However, the individual level values from six individuals—five of them showed pain related comorbidity besides depression—fell within the lower pathological range. There was no correlation between Hamilton depression scale and the attractor attributes (δM and δD). Discussion: Depression does not affect gait as motor fatigability does in pwMS. Results from subjects with pain during the treadmill test show a moderately increased variability and moderately altered attractors.
文摘Mutations leading to constitutive activation of the Wnt pathway and its target genes are frequently observed in cancer. The Wnt pathway promotes cell proliferation and increasing evidence supports its role also in cancer cell metabolism. This study aims to elucidate the role of the Wnt/β-catenin target gene CCND1 in these processes in colorectal cancer. We analyzed whether knock-down of CCND1 affects cell cycle progression and energy metabolism in a colorectal cancer cell line. Down-regulation of CCND1 led to retardation of the cell cycle. The proportion of cells in the G0 phase increased, while the amount of cells in the S- and G2/M phase decreased. Interestingly, knock-down of CCND1 changed the perinuclear localization of mitochondria into a homogeneous distribution within the cytosol. In addition CCND1 knock-down led to an increase of the intracellular ATP level indicating that cyclin D1 reduced mitochondrial activity. Our findings suggest that in addition to its role in cell cycle regulation, the Wnt target gene CCND1 regulates mitochondrial localization and inhibits mitochondrial activity in colorectal cancer cells.
