Local government performance and democratic consolidation: Explaining ordinance proposal in Busan Metropolitan Council

This article assesses the role of local councils as a conduit for democratic consolidation through the examination of the legislative performance of the members of a South Korean metropolitan city council. We collected data on ordinance proposals in Busan Metropolitan Council from 2006 to 2018 (the 5th to 7th Councils) and analysed, first, the effects of individual attributes of local council members on legislative performance through negative binomial model analysis and, second, the effects of legislative networks on council members' performance. Three findings contribute to the literature: first, the number of proposed ordinances by council members increased over time, while those by the mayor decreased in the same period, suggesting an erosion of executive dominance of policymaking in local councils. Second, female and newly elected council members are most active in legislative proposals, which underlines that these members are more connected to the electorate than long-serving incumbents. Third, network analyses show increasingly diverse and multi-centred communities behind ordinance proposals; this suggests a move from personalistic politics to institutionalised politics.National Research Foundation of Korea, Grant/Award Number: NRF2018S1A5A2A03033767; Ministry of Education of the Republic of Kore

Iron Insufficiency Compromises Motor Neurons and Their Mitochondrial Function in Irp2-Null Mice

Genetic ablation of Iron Regulatory Protein 2 (Irp2, Ireb2), which post-transcriptionally regulates iron metabolism genes, causes a gait disorder in mice that progresses to hind-limb paralysis. Here we have demonstrated that misregulation of iron metabolism from loss of Irp2 causes lower motor neuronal degeneration with significant spinal cord axonopathy. Mitochondria in the lumbar spinal cord showed significantly decreased Complex I and II activities, and abnormal morphology. Lower motor neurons appeared to be the most adversely affected neurons, and we show that functional iron starvation due to misregulation of iron import and storage proteins, including transferrin receptor 1 and ferritin, may have a causal role in disease. We demonstrated that two therapeutic approaches were beneficial for motor neuron survival. First, we activated a homologous protein, IRP1, by oral Tempol treatment and found that axons were partially spared from degeneration. Secondly, we genetically decreased expression of the iron storage protein, ferritin, to diminish functional iron starvation. These data suggest that functional iron deficiency may constitute a previously unrecognized molecular basis for degeneration of motor neurons in mice

Iron Insufficiency Compromises Motor Neurons and Their Mitochondrial Function in \u3ci\u3eIrp2\u3c/i\u3e-Null Mice

Genetic ablation of Iron Regulatory Protein 2 (Irp2, Ireb2), which post-transcriptionally regulates iron metabolism genes, causes a gait disorder in mice that progresses to hind-limb paralysis. Here we have demonstrated that misregulation of iron metabolism from loss of Irp2 causes lower motor neuronal degeneration with significant spinal cord axonopathy. Mitochondria in the lumbar spinal cord showed significantly decreased Complex I and II activities, and abnormal morphology. Lower motor neurons appeared to be the most adversely affected neurons, and we show that functional iron starvation due to misregulation of iron import and storage proteins, including transferrin receptor 1 and ferritin, may have a causal role in disease. We demonstrated that two therapeutic approaches were beneficial for motor neuron survival. First, we activated a homologous protein, IRP1, by oral Tempol treatment and found that axons were partially spared from degeneration. Secondly, we genetically decreased expression of the iron storage protein, ferritin, to diminish functional iron starvation. These data suggest that functional iron deficiency may constitute a previously unrecognized molecular basis for degeneration of motor neurons in mice

Deletion of Iron Regulatory Protein 1 Causes Polycythemia and Pulmonary Hypertension in Mice through Translational Derepression of HIF2α

Iron regulatory proteins (Irps) 1 and 2 posttranscriptionally control the expression of transcripts that contain iron-responsive element (IRE) sequences, including ferritin, ferroportin, transferrin receptor, and hypoxia-inducible factor 2α (HIF2α). We report here that mice with targeted deletion of Irp1 developed pulmonary hypertension and polycythemia that was exacerbated by a low-iron diet. Hematocrits increased to 65% in iron-starved mice, and many polycythemic mice died of abdominal hemorrhages. Irp1 deletion enhanced HIF2α protein expression in kidneys of Irp1(-/-) mice, which led to increased erythropoietin (EPO) expression, polycythemia, and concomitant tissue iron deficiency. Increased HIF2α expression in pulmonary endothelial cells induced high expression of endothelin-1, likely contributing to the pulmonary hypertension of Irp1(-/-) mice. Our results reveal why anemia is an early physiological consequence of iron deficiency, highlight the physiological significance of Irp1 in regulating erythropoiesis and iron distribution, and provide important insights into the molecular pathogenesis of pulmonary hypertension

Corporate governance under proportional electoral systems

Electoral systems, Proportional representation systems, Electoral threshold, Corporate governance, Minority shareholder protection,