Mortality transition and differential incentives for early retirement

Many studies specify human mortality patterns parametrically, with a parameter change affecting mortality rates at different ages simultaneously. Motivated by the stylized fact that a mortality decline affects primarily younger people in the early phase of mortality transition but mainly older people in the later phase, we study how a mortality change at an arbitrary age affects optimal retirement age. Using the Volterra derivative for a functional, we show that mortality reductions at older ages delay retirement unambiguously, but that mortality reductions at younger ages may lead to earlier retirement due to a substantial increase in the individual's expected lifetime human wealth. © 2011 Elsevier Inc.postprin

Education, lifetime labor supply, and longevity improvements

This paper presents an analysis of the differential role of mortality for the optimal schooling and retirement age when the accumulation of human capital follows the so-called “Ben-Porath mechanism”. We set up a life-cycle model of consumption and labor supply at the extensive margin that allows for endogenous human capital formation. This paper makes two important contributions. First, we provide the conditions under which a decrease in mortality leads to a longer education period and an earlier retirement age. Second, those conditions are decomposed into a Ben-Porath mechanism and a lifetime-human wealth effect vs. the years-to-consume effect. Finally, using US and Swedish data for cohorts born between 1890 and 2000, we show that our model can match the empirical evidence

The ER-Bound RING Finger Protein 5 (RNF5/RMA1) Causes Degenerative Myopathy in Transgenic Mice and Is Deregulated in Inclusion Body Myositis

Growing evidence supports the importance of ubiquitin ligases in the pathogenesis of muscular disorders, although underlying mechanisms remain largely elusive. Here we show that the expression of RNF5 (aka RMA1), an ER-anchored RING finger E3 ligase implicated in muscle organization and in recognition and processing of malfolded proteins, is elevated and mislocalized to cytoplasmic aggregates in biopsies from patients suffering from sporadic-Inclusion Body Myositis (sIBM). Consistent with these findings, an animal model for hereditary IBM (hIBM), but not their control littermates, revealed deregulated expression of RNF5. Further studies for the role of RNF5 in the pathogenesis of s-IBM and more generally in muscle physiology were performed using RNF5 transgenic and KO animals. Transgenic mice carrying inducible expression of RNF5, under control of β-actin or muscle specific promoter, exhibit an early onset of muscle wasting, muscle degeneration and extensive fiber regeneration. Prolonged expression of RNF5 in the muscle also results in the formation of fibers containing congophilic material, blue-rimmed vacuoles and inclusion bodies. These phenotypes were associated with altered expression and activity of ER chaperones, characteristic of myodegenerative diseases such as s-IBM. Conversely, muscle regeneration and induction of ER stress markers were delayed in RNF5 KO mice subjected to cardiotoxin treatment. While supporting a role for RNF5 Tg mice as model for s-IBM, our study also establishes the importance of RNF5 in muscle physiology and its deregulation in ER stress associated muscular disorders

Optimal prevention and elimination of infectious diseases

This article studies the optimal intertemporal allocation of resources devoted to the prevention of deterministic infectious diseases that admit an endemic steady-state. Under general assumptions, the optimal control problem is shown to be formally similar to an optimal growth model with endogenous discounting. The optimal dynamics then depends on the interplay between the epidemiological characteristics of the disease, the labor productivity and the degree of intergenerational equity. Phase diagrams analysis reveals that multiple trajectories, which converge to endemic steady-states with or without prevention or to the elimination of the disease, are feasible. Elimination implies initially a larger prevention than in other trajectories, but after a finite date, prevention is equal to zero. This “sooner-the-better” strategy is shown to be optimal if the pure discount rate is sufficiently low. © 2021 Elsevier B.V

Recurrent amplification of grid‐cell activity

High-level cognitive abilities such as navigation and spatial memory are thought to rely on the activity of grid cells in the medial entorhinal cortex (MEC), which encode the animal's position in space with periodic triangular patterns. Yet the neural mechanisms that underlie grid-cell activity are still unknown. Recent in vitro and in vivo experiments indicate that grid cells are embedded in highly structured recurrent networks. But how could recurrent connectivity become structured during development? And what is the functional role of these connections? With mathematical modeling and simulations, we show that recurrent circuits in the MEC could emerge under the supervision of weakly grid-tuned feedforward inputs. We demonstrate that a learned excitatory connectivity could amplify grid patterns when the feedforward sensory inputs are available and sustain attractor states when the sensory cues are lost. Finally, we propose a Fourier-based measure to quantify the spatial periodicity of grid patterns: the grid-tuning index.Peer Reviewe