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"Salin, Pascal"
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The Monetary Economics of the Austrian School and the Chicago School
To what extent is there complementarity or agreement between Austrian economics and the Chicago school on monetary issues? Both Austrians and Chicagoans would agree that monetary expansion has real effects in the short run, though they emphasize different variables. In the long run, Austrians argue that there is a lasting real effect of monetary expansion—money is not neutral—but Chicagoans too argue that economic activity is less efficient even if people correctly forecast the rate of inflation. Regarding the balance of payments, both the Austrian and Chicago school lead to the conclusion that there can be no balance-of-payments problem. Both are modern versions of the classical price specie flow theory. Perhaps the Austrian approach to monetary economics and the Chicago school approach are more compatible than is commonly thought.
Journal Article
The international monetary system and the theory of monetary systems
The international monetary system, and the disparate systems that make it up, are complex and there are many fallacies surrounding the ways in which they work. This book provides a clear and rigorous understanding of these systems and their possible consequences.
Book
On Understanding France and the French Situation
The French social model is mainly a model of state interventionism, which creates a strange contrast between two things: the fact that France is a collectivized society and the fact that it has produced some of the most famous and important libertal intellectuals (for instance, Turgot, Bastiat, and Jean-Baptiste Say). We are inclined to wonder why these liberal writers--who are famous all around the world--have not been able to convince French people so that France would be a model of liberalism.
Journal Article
TP53INP1 exerts neuroprotection under ageing and Parkinson’s disease-related stress condition
TP53INP1 is a stress-induced protein, which acts as a dual positive regulator of transcription and of autophagy and whose deficiency has been linked with cancer and metabolic syndrome. Here, we addressed the unexplored role of TP53INP1 and of its
Drosophila
homolog dDOR in the maintenance of neuronal homeostasis under chronic stress, focusing on dopamine (DA) neurons under normal ageing- and Parkinson’s disease (PD)-related context.
Trp53inp1
−
/
−
mice displayed additional loss of DA neurons in the substantia nigra compared to wild-type (WT) mice, both with ageing and in a PD model based on targeted overexpression of α-synuclein. Nigral
Trp53inp1
expression of WT mice was not significantly modified with ageing but was markedly increased in the PD model.
Trp53inp2
expression showed similar evolution and did not differ between WT and
Trp53inp1
−
/
−
mice. In
Drosophila
, pan-neuronal
dDOR
overexpression improved survival under paraquat exposure and mitigated the progressive locomotor decline and the loss of DA neurons caused by the human α-synuclein A30P variant.
dDOR
overexpression in DA neurons also rescued the locomotor deficit in flies with RNAi-induced downregulation of
dPINK1
or
dParkin
. Live imaging, confocal and electron microscopy in fat bodies, neurons, and indirect flight muscles showed that
dDOR
acts as a positive regulator of basal autophagy and mitophagy independently of the PINK1-mediated pathway. Analyses in a mammalian cell model confirmed that modulating
TP53INP1
levels does not impact mitochondrial stress-induced PINK1/Parkin-dependent mitophagy. These data provide the first evidence for a neuroprotective role of TP53INP1/dDOR and highlight its involvement in the regulation of autophagy and mitophagy in neurons.
Journal Article
Targeted Tshz3 deletion in corticostriatal circuit components segregates core autistic behaviors
We previously linked
TSHZ3
haploinsufficiency to autism spectrum disorder (ASD) and showed that embryonic or postnatal
Tshz3
deletion in mice results in behavioral traits relevant to the two core domains of ASD, namely social interaction deficits and repetitive behaviors. Here, we provide evidence that cortical projection neurons (CPNs) and striatal cholinergic interneurons (SCINs) are two main and complementary players in the TSHZ3-linked ASD syndrome. In the cerebral cortex, TSHZ3 is expressed in CPNs and in a proportion of GABAergic interneurons, but not in cholinergic interneurons or glial cells. In the striatum, TSHZ3 is expressed in all SCINs, while its expression is absent or partial in the other main brain cholinergic systems. We then characterized two new conditional knockout (cKO) models generated by crossing
Tshz3
flox/flox
with
Emx1-Cre
(
Emx1-cKO
) or
Chat-Cre
(
Chat-cKO
) mice to decipher the respective role of CPNs and SCINs.
Emx1-cKO
mice show altered excitatory synaptic transmission onto CPNs and impaired plasticity at corticostriatal synapses, with neither cortical neuron loss nor abnormal layer distribution. These animals present social interaction deficits but no repetitive patterns of behavior.
Chat-cKO
mice exhibit no loss of SCINs but changes in the electrophysiological properties of these interneurons, associated with repetitive patterns of behavior without social interaction deficits. Therefore, dysfunction in either CPNs or SCINs segregates with a distinct ASD behavioral trait. These findings provide novel insights onto the implication of the corticostriatal circuitry in ASD by revealing an unexpected neuronal dichotomy in the biological background of the two core behavioral domains of this disorder.
Journal Article
Correction: Targeted Tshz3 deletion in corticostriatal circuit components segregates core autistic behaviors
We previously linked TSHZ3 haploinsufficiency to autism spectrum disorder (ASD) and showed that embryonic or postnatal Tshz3 deletion in mice results in behavioral traits relevant to the two core domains of ASD, namely social interaction deficits and repetitive behaviors. Here, we provide evidence that cortical projection neurons (CPNs) and striatal cholinergic interneurons (SCINs) are two main and complementary players in the TSHZ3-linked ASD syndrome. In the cerebral cortex, TSHZ3 is expressed in CPNs and in a proportion of GABAergic interneurons, but not in cholinergic interneurons or glial cells. In the striatum, TSHZ3 is expressed in all SCINs, while its expression is absent or partial in the other main brain cholinergic systems. We then characterized two new conditional knockout (cKO) models generated by crossing Tshz3 flox/flox with Emx1-Cre (Emx1-cKO) or Chat-Cre (Chat-cKO) mice to decipher the respective role of CPNs and SCINs. Emx1-cKO mice show altered excitatory synaptic transmission onto CPNs and impaired plasticity at corticostriatal synapses, with neither cortical neuron loss nor abnormal layer distribution. These animals present social interaction deficits but no repetitive patterns of behavior. Chat-cKO mice exhibit no loss of SCINs but changes in the electrophysiological properties of these interneurons, associated with repetitive patterns of behavior without social interaction deficits. Therefore, dysfunction in either CPNs or SCINs segregates with a distinct ASD behavioral trait. These findings provide novel insights onto the implication of the corticostriatal circuitry in ASD by revealing an unexpected neuronal dichotomy in the biological background of the two core behavioral domains of this disorder.
Journal Article
Enhanced differentiation of human induced pluripotent stem cells toward the midbrain dopaminergic neuron lineage through GLYPICAN‐4 downregulation
Enhancing the differentiation potential of human induced pluripotent stem cells (hiPSC) into disease‐relevant cell types is instrumental for their widespread application in medicine. Here, we show that hiPSCs downregulated for the signaling modulator GLYPICAN‐4 (GPC4) acquire a new biological state characterized by increased hiPSC differentiation capabilities toward ventral midbrain dopaminergic (VMDA) neuron progenitors. This biological trait emerges both in vitro, upon exposing cells to VMDA neuronal differentiation signals, and in vivo, even when transplanting hiPSCs at the extreme conditions of floor‐plate stage in rat brains. Moreover, it is compatible with the overall neuronal maturation process toward acquisition of substantia nigra neuron identity. HiPSCs with downregulated GPC4 also retain self‐renewal and pluripotency in stemness conditions, in vitro, while losing tumorigenesis in vivo as assessed by flank xenografts. In conclusion, our results highlight GPC4 downregulation as a powerful approach to enhance generation of VMDA neurons. Outcomes may contribute to establish hiPSC lines suitable for translational applications.
Schematic representation of the functional properties acquired by human induced pluripotent stem cells (hiPSCs) following GLYPICAN‐4 (GPC4) downregulation versus control. This includes impaired in vivo tumorigenesis as assessed by flank xenografts, and enhanced differentiation toward ventral midbrain dopaminergic (VMDA) neuron progenitors both in vitro and upon brain transplantation.
Journal Article
Striatal Molecular Signature of Subchronic Subthalamic Nucleus High Frequency Stimulation in Parkinsonian Rat
This study addresses the molecular mechanisms underlying the action of subthalamic nucleus high frequency stimulation (STN-HFS) in the treatment of Parkinson's disease and its interaction with levodopa (L-DOPA), focusing on the striatum. Striatal gene expression profile was assessed in rats with nigral dopamine neuron lesion, either treated or not, using agilent microarrays and qPCR verification. The treatments consisted in anti-akinetic STN-HFS (5 days), chronic L-DOPA treatment inducing dyskinesia (LIDs) or the combination of the two treatments that exacerbated LIDs. STN-HFS modulated 71 striatal genes. The main biological processes associated with the differentially expressed gene products include regulation of growth, of apoptosis and of synaptic transmission, and extracellular region is a major cellular component implicated. In particular, several of these genes have been shown to support survival or differentiation of striatal or of dopaminergic neurons. These results indicate that STN HFS may induce widespread anatomo-functional rearrangements in the striatum and create a molecular environment favorable for neuroprotection and neuroplasticity. STN-HFS and L-DOPA treatment share very few common gene regulation features indicating that the molecular substrates underlying their striatal action are mostly different; among the common effects is the down-regulation of Adrb1, which encodes the adrenergic beta-1-receptor, supporting a major role of this receptor in Parkinson's disease. In addition to genes already reported to be associated with LIDs (preprodynorphin, thyrotropin-releasing hormone, metabotropic glutamate receptor 4, cannabinoid receptor 1), the comparison between DOPA and DOPA/HFS identifies immunity-related genes as potential players in L-DOPA side effects.
Journal Article
Why Hayek is Right against Keynes?
It is argued in that paper that Hayek came out the winner in the debate opposing him to Keynes. Keynes argued in favour of specific economic policies without a prior analysis of the causes of business cycles. His discussion of economic policy is backed on an
account of cycles that would, according to him, be based on the irrationality of economic actors and the non-effectiveness of price adjustments. As a result, he says, quantities have to adjust which leads to unemployment. Hayek and the Austrians propose, by contrast, a well-articulated theory of business cycles rooted in a micro-economic approach (agents are rational, albeit badly informed). This leads them to identify the source of the cycle in monetary shocks. In our modern economies, as in the Austrian theory, economic policies conducted by the states are the main driver of the cycles. The consequences of this analysis in terms of economic policy are clear: When excessive regulation and fiscal burden cause a recession the solution must be found in tax cuts and deregulation, not in (Keynesian) monetary or fiscal policies that will do nothing but foster mal-investment.
Journal Article