The effects of interbank networks on efficiency and stability in a macroeconomic agent-based model

We develop a macroeconomic agent-based model that consists of firms, banks, unions and households who interact on labour, goods, credit and interbank markets. The model endogenises pricing decisions by firms, wage setting by unions and interest rate setting by banks on both firm and interbank lending. Banks also set leverage targets and precautionary liquidity buffers on the basis of internal risk models. Our model produces endogenous fluctuations driven by the pricing behaviour of firms and the wage setting behaviour of unions. Fluctuations lead to loan defaults which are exacerbated as lenders reduce lending and charge higher interest rates, inducing a credit crunch. We also study how making the inter-banking network more connected affects the key outcomes of the economy and find that while the flow of funds from surplus banks to firms can be increased, the latter effect is soon dominated by increasing instability in the real sector as firms default at higher rates. While the banking sector experiences fewer defaults as a whole, losses on the interbank market increase as a source of bank defaults

Exploiting Intrinsic Kinematic Null Space for Supernumerary Robotic Limbs Control

Supernumerary robotic limbs (SRLs) gained increasing interest in the last years for their applicability as healthcare and assistive technologies. These devices can either support or augment human sensorimotor capabilities, allowing users to complete tasks that are more complex than those feasible for their natural limbs. However, for a successful coordination between natural and artificial limbs, intuitiveness of interaction and perception of autonomy are key enabling features, especially for people suffering from motor disorders and impairments. The development of suitable human-robot interfaces is thus fundamental to foster the adoption of SRLs.With this work, we describe how to control an extra degree of freedom by taking advantage of what we defined the Intrinsic Kinematic Null Space, i.e. the redundancy of the human kinematic chain involved in the ongoing task. Obtained results demonstrated that the proposed control strategy is effective for performing complex tasks with a supernumerary robotic finger, and that practice improves users' control ability

The intellectual disability protein RAB39B selectively regulates GluA2 trafficking to determine synaptic AMPAR composition

RAB39B is a member of the RAB family of small GTPases that controls intracellular vesicular trafficking in a compartment-specific manner. Mutations in the RAB39B gene cause intellectual disability comorbid with autism spectrum disorder and epilepsy, but the impact of RAB39B loss of function on synaptic activity is largely unexplained. Here we show that protein interacting with C-kinase 1 (PICK1) is a downstream effector of GTP-bound RAB39B and that RAB39B-PICK1 controls trafficking from the endoplasmic reticulum to the Golgi and, hence, surface expression of GluA2, a subunit of alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptors (AMPARs). The role of AMPARs in synaptic transmission varies depending on the combination of subunits (GluA1, GluA2 and GluA3) they incorporate. RAB39B downregulation in mouse hippocampal neurons skews AMPAR composition towards non GluA2-containing Ca(2+)-permeable forms and thereby alters synaptic activity, specifically in hippocampal neurons. We posit that the resulting alteration in synaptic function underlies cognitive dysfunction in RAB39B-related disorders

Age-related cognitive and motor decline in a mouse model of CDKL5 deficiency disorder is associated with increased neuronal senescence and death

open20noThis work was supported by grants to E.C. and M.G. from Telethon (GGP19045) and from the Italian parent Association “CDKL5 insieme verso la cura”, and to M.G. from the Association “l’Albero di Greta”, from the International Foundation for CDKL5 Research (IFCR 2019), from the CDKL5 Program of Excellence - LouLou Fundation (CDKL5-17-106-01) and from the Association Française du Syndrome de Rett (ASFR 2017).CDKL5 deficiency disorder (CDD) is a severe neurodevelopmental disease caused by mutations in the X-linked CDKL5 gene. Children affected by CDD display a clinical phenotype characterized by early-onset epilepsy, intellectual disability, motor impairment, and autistic-like features. Although the clinical aspects associated with CDKL5 mutations are well described in children, adults with CDD are still under-characterized. Similarly, most animal research has been carried out on young adult Cdkl5 knockout (KO) mice only. Since age represents a risk factor for the worsening of symptoms in many neurodevelopmental disorders, understanding age differences in the development of behavioral deficits is crucial in order to optimize the impact of therapeutic interventions. Here, we compared young adult Cdkl5 KO mice with middle-aged Cdkl5 KO mice, at a behavioral, neuroanatomical, and molecular level. We found an age-dependent decline in motor, cognitive, and social behaviors in Cdkl5 KO mice, as well as in breathing and sleep patterns. The behavioral decline in older Cdkl5 KO mice was not associated with a worsening of neuroanatomical alterations, such as decreased dendritic arborization or spine density, but was paralleled by decreased neuronal survival in different brain regions such as the hippocampus, cortex, and basal ganglia. Interestingly, we found increased β-galactosidase activity and DNA repair protein levels, γH2AX and XRCC5, in the brains of older Cdkl5 KO mice, which suggests that an absence of Cdkl5 accelerates neuronal senescence/death by triggering irreparable DNA damage. In summary, this work provides evidence that CDKL5 may play a fundamental role in neuronal survival during brain aging and suggests a possible worsening with age of the clinical picture in CDD patients.openGennaccaro L.; Fuchs C.; Loi M.; Pizzo R.; Alvente S.; Berteotti C.; Lupori L.; Sagona G.; Galvani G.; Gurgone A.; Raspanti A.; Medici G.; Tassinari M.; Trazzi S.; Ren E.; Rimondini R.; Pizzorusso T.; Zoccoli G.; Giustetto M.; Ciani E.Gennaccaro L.; Fuchs C.; Loi M.; Pizzo R.; Alvente S.; Berteotti C.; Lupori L.; Sagona G.; Galvani G.; Gurgone A.; Raspanti A.; Medici G.; Tassinari M.; Trazzi S.; Ren E.; Rimondini R.; Pizzorusso T.; Zoccoli G.; Giustetto M.; Ciani E

The PRIAMO study: age- and sex-related relationship between prodromal constipation and disease phenotype in early Parkinson's disease.

OBJECTIVES: To explore the impact of sex and age on relationship between prodromal constipation and disease phenotype in Parkinson's disease at early stages. METHODS: A total of 385 Parkinson's disease patients from the PRIAMO study were classified according to the presence of prodromal constipation and followed for 24 months. Multivariable mixed-effect models were applied. All analyses were performed separately for sex (64.1% men) and median age (different by sex: 67 years-old in men and 68 years-old in women). RESULTS: As for sex, prodromal constipation was associated with greater odds of attention/memory complaints and apathy symptoms in women only. As for age, prodromal constipation was associated with lower cognitive and higher apathy scores in older patients only. CONCLUSIONS: Prodromal constipation anticipates lower cognitive performances and more severe apathy since the earliest stages in women and older patients. Sex- and age-related heterogeneity of prodromal markers of Parkinson's disease may impact disease phenotype

Enter the MATRIX model: a Multi-Agent model for Transition Risks with application to energy shocks

The global energy crisis that began in fall 2021 and the subsequent spike in energy prices constitute a significant challenge for the world economy that risks undermining the postCOVID-19 recovery. In this paper, we develop and calibrate a new Multi-Agent model for Transition Risks (MATRIX) to analyze the role of energy in the functioning of a complex adaptive system and the economic and distributional effects of energy shocks. The economic system is populated by heterogeneous agents, i.e., households, firms and banks, which take optimal decision rules and interact in decentralized markets characterized by limited information. After calibrating the model on US quarterly macroeconomic data, we assess the economic and distributional impacts of different types of energy shocks, namely: (i) an exogenous increase in the price of fossil fuels (e.g., oil or gas); (ii) a decrease in energy firms' productivity; (iii) a reduction in the available quantity of fossil fuels. We find that the energy shocks entail similar effects at the aggregate level in terms of higher inflation and lower real GDP. Nevertheless, the distribution of gains and losses across sectors and agents varies significantly depending on the type of shock. Our findings suggest that policymakers should carefully consider the nature of energy shocks and the resulting distributional effects to design effective measures in response to energy crises.(c) 2022 Elsevier B.V. All rights reserved