The paradoxical and time-varying effects of family ownership on absorptive capacity

We present a theory of family ownership as a driver of the heterogeneity (between-firm differences) and variability (within-firm differences over time) of absorptive capacity (AC). We introduce the concepts of motivation and implementation gaps to explain why, paradoxically, family ownership can cause both upward and downward divergences in AC

Protecting backaction-evading measurements from parametric instability

Noiseless measurement of a single quadrature in systems of parametrically coupled oscillators is theoretically possible by pumping at the sum and difference frequencies of the two oscillators, realizing a backaction-evading (BAE) scheme. Although this would hold true in the simplest scenario for a system with pure three-wave mixing, implementations of this scheme are hindered by unwanted higher-order parametric processes that destabilize the system and add noise. We show analytically that detuning the two pumps from the sum and difference frequencies can stabilize the system and fully recover the BAE performance, enabling operation at otherwise inaccessible cooperativities. We also show that the acceleration demonstrated in a weak signal detection experiment [PRX QUANTUM 4, 020302 (2023)] was only achievable because of this detuning technique.Comment: 7 pages, 3 figure

Overexpression of Extracellular Superoxide Dismutase Protects against Brain Injury Induced by Chronic Hypoxia

Extracellular superoxide dismutase (EC-SOD) is an isoform of SOD normally found both intra- and extra-cellularly and accounting for most SOD activity in blood vessels. Here we explored the role of EC-SOD in protecting against brain damage induced by chronic hypoxia. EC-SOD Transgenic mice, were exposed to hypoxia (FiO2.1%) for 10 days (H-KI) and compared to transgenic animals housed in room air (RA-KI), wild type animals exposed to hypoxia (H-WT or wild type mice housed in room air (RA-WT). Overall brain metabolism evaluated by positron emission tomography (PET) showed that H-WT mice had significantly higher uptake of (18)FDG in the brain particularly the hippocampus, hypothalamus, and cerebellum. H-KI mice had comparable uptake to the RA-KI and RA-WT groups. To investigate the functional state of the hippocampus, electrophysiological techniques in ex vivo hippocampal slices were performed and showed that H-KI had normal synaptic plasticity, whereas H-WT were severely affected. Markers of oxidative stress, GFAP, IBA1, MIF, and pAMPK showed similar values in the H-KI and RA-WT groups, but were significantly increased in the H-WT group. Caspase-3 assay and histopathological studies showed significant apoptosis/cell damage in the H-WT group, but no significant difference in the H-KI group compared to the RA groups. The data suggest that EC-SOD has potential prophylactic and therapeutic roles in diseases with compromised brain oxygenation

Assessing the impact of a community-based pro-active monitoring program addressing the need for care of community-dwelling citizens aged more than 80: protocol for a prospective pragmatic trial and results of the baseline Assessment

The aim of this paper is to describe the protocol of a study assessing the impact of a Community-based pro-Active Monitoring Program, by measuring the effect in counteracting the adverse outcomes related to frailty

Neu3 Activity Enhances Egfr Activation Without Affecting Egfr Expression

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Loss of the nucleoporin Aladin in central nervous system and fibroblasts of Allgrove Syndrome

Allgrove syndrome (AS) is a rare disease with broad neurological involvement. Neurodegeneration can affect spinal motor neurons, Purkinje cells, striatal neurons, and the autonomic system. The mechanisms that lead to neuronal loss are still unclear. Recessive mutations in the AAAS gene affect the encoded protein Aladin, which would normally localize to the cytoplasmic face of the nuclear membrane as part of the nuclear pore complex (NPC). While the NPC is known to be a key factor for nucleo-cytoplasmic transport, the precise role of Aladin has not been elucidated yet. Here, we explored the consequences of the homozygous AAAS mutation c.464G>A (p.R155H) in central nervous system tissues and fibroblasts of a novel AS patient presenting motor neuron disease, cerebellar ataxia, and autonomic dysfunction. Neuropathological analyses showed severe loss of motor neurons and Purkinje cells, with significant reduction in the perinuclear expression of Aladin. A reduced amount of protein was detected in the nuclear membrane fraction of the patient's brain. RNA analysis revealed a significant reduction of the transcript AAAS-1, while the AAAS-2 transcript was upregulated in fibroblasts. To our knowledge, this is the first study to demonstrate the effects of AAAS mutations in human central nervous system