Basic income and the right to work: a Keynesian approach

Among the proposals for radical reform of social policy are basic income, which would pay an unconditional cash benefit to all individuals, and the right to work, which would offer guaranteed employment arranged by the state if necessary. This paper examines the macroeconomic consequences of such reform proposals. It sets up a simple Keynesian income-expenditure model that includes basic income and the right to work as alternative methods of providing social assistance, along with the more traditional approach of paying unemployment benefits. The various schemes are compared and contrasted with regard to their implications for employment, stability, distribution, efficiency and the government budget. Potential benefits of basic income or the right to work are emphasised, despite the political obstacles to implementing them

Intra-Aortic Balloon Counterpulsation for the Treatment of Ischemic Stroke

Colloid volume expansion has been shown to increase cerebral blood flow to ischemic brain in an animal stroke model and improve recovery in patients. It is, however, potentially hazardous to use in older patients because of frequently associated cardiovascular disease. Intra-Aortic Balloon Counterpulsation might reduce the risks of using volume expansion therapy in the elderly patient. This study was designed to see if Intra-Aortic Balloon Counterpulsation (without volume expansion), in an animal with a normal heart, would increase cerebral blood flow and EEG activity in the ischemic brain. Unilateral cerebral ischemia was produced in baboons (n = 9) after right middle cerebral artery occlusion. A 12 ml intra-aortic balloon catheter was introduced into the descending aorta via the femoral artery prior to middle cerebral artery occlusion. The balloon was positioned distal to the origin of the left subclavian artery and following middle cerebral artery occlusion was inflated with each R wave on the ECG. Cardiac output, cerebral blood flow (by Hydrogen wash-out), computer-mapped EEG, and hemodynamic data were collected prior to middle cerebral artery occlusion and following occlusion both before and during counterpulsation. Intra-Aortic Balloon Counterpulsation produced a significant increase in pulse pressure from 54.7 ± 21 to 70.6 ± 33 mmHg (p = .043). No significant change was seen in cardiac output, mean arterial pressure, or cerebral blood flow. Although the computer- mapped EEG improved and the right (ischemic) hemisphere cerebral blood flow did increase slightly from 16.9 ± 6.5 to 18.3 ± 8.3 ml/100 gm/min, the cerebral blood flow changes were not significant (p=.295). It is possible that the desired increase in cerebral blood flow was not achieved partly because the animals were only 3-4 years old and were difficult to stroke. We believe that there is merit to a follow-up study in older primates with colloid volume expansion where Intra-Aortic Balloon Counterpulsation is used to protect the heart from the deleterious effects of volume expansion and where the cardiac effects of volume expansion and counterpulsation are quantified. Perhaps volume expansion with Intra-Aortic Balloon Counterpulsation will be safer and more effective than either treatment modality alone. (All data reported as mean ± standard deviation

Reverse engineering a mouse embryonic stem cell-specific transcriptional network reveals a new modulator of neuronal differentiation

Gene expression profiles can be used to infer previously unknown transcriptional regulatory interaction among thousands of genes, via systems biology ‘reverse engineering’ approaches. We ‘reverse engineered’ an embryonic stem (ES)-specific transcriptional network from 171 gene expression profiles, measured in ES cells, to identify master regulators of gene expression (‘hubs’). We discovered that E130012A19Rik (E13), highly expressed in mouse ES cells as compared with differentiated cells, was a central ‘hub’ of the network. We demonstrated that E13 is a protein-coding gene implicated in regulating the commitment towards the different neuronal subtypes and glia cells. The overexpression and knock-down of E13 in ES cell lines, undergoing differentiation into neurons and glia cells, caused a strong up-regulation of the glutamatergic neurons marker Vglut2 and a strong down-regulation of the GABAergic neurons marker GAD65 and of the radial glia marker Blbp. We confirmed E13 expression in the cerebral cortex of adult mice and during development. By immuno-based affinity purification, we characterized protein partners of E13, involved in the Polycomb complex. Our results suggest a role of E13 in regulating the division between glutamatergic projection neurons and GABAergic interneurons and glia cells possibly by epigenetic-mediated transcriptional regulation

Reverse engineering a mouse embryonic stem cell-specific transcriptional network reveals a new modulator of neuronal differentiation

Gene expression profiles can be used to infer previously unknown transcriptional regulatory interaction among thousands of genes, via systems biology 'reverse engineering' approaches. We 'reverse engineered' an embryonic stem (ES)-specific transcriptional network from 171 gene expression profiles, measured in ES cells, to identify master regulators of gene expression ('hubs'). We discovered that E130012A19Rik (E13), highly expressed in mouse ES cells as compared with differentiated cells, was a central 'hub' of the network. We demonstrated that E13 is a protein-coding gene implicated in regulating the commitment towards the different neuronal subtypes and glia cells. The overexpression and knock-down of E13 in ES cell lines, undergoing differentiation into neurons and glia cells, caused a strong up-regulation of the glutamatergic neurons marker Vglut2 and a strong down-regulation of the GABAergic neurons marker GAD65 and of the radial glia marker Blbp. We confirmed E13 expression in the cerebral cortex of adult mice and during development. By immuno-based affinity purification, we characterized protein partners of E13, involved in the Polycomb complex. Our results suggest a role of E13 in regulating the division between glutamatergic projection neurons and GABAergic interneurons and glia cells possibly by epigenetic-mediated transcriptional regulation

Reverse engineering a mouse embryonic stem cell-specific transcriptional network reveals a new modulator of neuronal differentiation

Gene expression profiles can be used to infer previously unknown transcriptional regulatory interaction among thousands of genes, via systems biology 'reverse engineering' approaches. We 'reverse engineered' an embryonic stem (ES)-specific transcriptional network from 171 gene expression profiles, measured in ES cells, to identify master regulators of gene expression ('hubs'). We discovered that E130012A19Rik (E13), highly expressed in mouse ES cells as compared with differentiated cells, was a central 'hub' of the network. We demonstrated that E13 is a protein-coding gene implicated in regulating the commitment towards the different neuronal subtypes and glia cells. The overexpression and knock-down of E13 in ES cell lines, undergoing differentiation into neurons and glia cells, caused a strong up-regulation of the glutamatergic neurons marker Vglut2 and a strong down-regulation of the GABAergic neurons marker GAD65 and of the radial glia marker Blbp. We confirmed E13 expression in the cerebral cortex of adult mice and during development. By immuno-based affinity purification, we characterized protein partners of E13, involved in the Polycomb complex. Our results suggest a role of E13 in regulating the division between glutamatergic projection neurons and GABAergic interneurons and glia cells possibly by epigenetic-mediated transcriptional regulation

A mouse embryonic stem cell bank for inducible overexpression of human chromosome 21 genes.

Abstract BACKGROUND: Dosage imbalance is responsible for several genetic diseases, among which Down syndrome is caused by the trisomy of human chromosome 21. RESULTS: To elucidate the extent to which the dosage imbalance of specific human chromosome 21 genes perturb distinct molecular pathways, we developed the first mouse embryonic stem (ES) cell bank of human chromosome 21 genes. The human chromosome 21-mouse ES cell bank includes, in triplicate clones, 32 human chromosome 21 genes, which can be overexpressed in an inducible manner. Each clone was transcriptionally profiled in inducing versus non-inducing conditions. Analysis of the transcriptional response yielded results that were consistent with the perturbed gene's known function. Comparison between mouse ES cells containing the whole human chromosome 21 (trisomic mouse ES cells) and mouse ES cells overexpressing single human chromosome 21 genes allowed us to evaluate the contribution of single genes to the trisomic mouse ES cell transcriptome. In addition, for the clones overexpressing the Runx1 gene, we compared the transcriptome changes with the corresponding protein changes by mass spectroscopy analysis. CONCLUSIONS: We determined that only a subset of genes produces a strong transcriptional response when overexpressed in mouse ES cells and that this effect can be predicted taking into account the basal gene expression level and the protein secondary structure. We showed that the human chromosome 21-mouse ES cell bank is an important resource, which may be instrumental towards a better understanding of Down syndrome and other human aneuploidy disorders

Quality control for biomarker determination in oncology: the experience of the Italian Network for Quality Assessment of Tumor Biomarkers (INQAT).

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