Corporate memory dynamics in project-based organizations (PBOs): multiple case study in Brazilian engineering design firms and a framework proposal

Purpose This study aims to investigate how the processes of memory acquisition, retention, retrieval and application occur in project-based organizations (PBOs). In this kind of organization, the nature of corporate memory is influenced by the transience, uniqueness and independence of the project portfolio. Such understanding may help practitioners to mitigate the effects of project transience and promote knowledge sharing among project teams. Design/methodology/approach An empirical and qualitative study was carried out through a multiple case study approach conducted in three Brazilian Engineering Design Firms, which are organized by projects. Document analysis, direct observation and semi-structured interviews with engineers, project managers and executives were conducted. Findings The memory acquisition process takes place in five forms which have different sources and destinations when comparing PBOs with traditional organizational settings. Memory retention in PBOs crosses organizational boundaries and establishes a knowledge network of former employees and third parties. The PBOs project memory can be divided into volatile and perennial memory, where the former can be lost throughout project execution and the latter is internalized, becoming an inseparable part of the corporate memory. Memory retrieval in PBOs is also distinct since it has particular mechanisms depending on whether the knowledge is technical or administrative. Originality/value The research investigates the corporate memory processes within the volatile context of PBOs in a Latin-American developing country whose culture favors tacit knowledge exchange. The paper proposes a framework that unveils different patterns of knowledge acquisition, temporary and perennial retention structures, intensive usage of external knowledge in memory retrieval and particular memory applications in PBOs. The framework may guide scholars, project managers, engineers and practitioners in navigating through the uniqueness of organizational learning flows and structures in PBOs

Baicalein Ameliorates Aβ-Induced Memory Deficits and Neuronal Atrophy via Inhibition of PDE2 and PDE4

Inhibition of phosphodiesterase 2 and 4 (PDE2A and PDE4) increases the intracellular cAMP and/or cGMP levels, which may prevent Amyloid β 42 oligomers (Aβ) related cognitive impairment and dementias. Baicalein, one of natural flavones found in the root of Scutellaria baicalensis Georgi, has a wide range of pharmacological activities including antioxidant and anti-inflammatory effects. However, no studies suggest whether baicalein mediated anti-Alzheimer’s disease (AD) events involve PDEs subtypes-mediated neuroprotective pathways. The present study examined whether memory enhancing effects of baicalein on Aβ- induced cognitive impairment are related to regulating neuroplasticity via PDE2 and PDE4 subtypes dependent cAMP/cGMP neuroprotective pathway. The results suggested that microinjected of Aβ into CA1 of hippocampus induced cognitive and memory impairment in mice, as evidenced by decreased recognition index in the novel object recognition (NOR) task, impaired memory acquisition, retention and retrieval in the Morris water maze (MWM) and shuttle box tests. These effects were reversed by treatment with baicalein for 14 days. Moreover, Aβ-induced neuronal atrophy and decreased expression of two synaptic proteins, synaptophysin and PSD 95, were prevented by baicalein. The increased expression of PDE2A and PDE4 subtypes (PDE4A, PDE4B and PDE4D), and decreased levels of cAMP/cGMP, pCREB/CREB and BDNF induced by Aβ were also blocked by chronic treatment of baicalein for 14 days. These findings suggest that baicalein’s reversal of Aβ-induced memory and cognitive disorder may involve the regulation of neuronal remodeling via regulation of PDE2/PDE4 subtypes related cAMP/cGMP -pCREB-BDNF pathway.

Role of hippocampal NF-κB and GluN2B in the memory acquisition impairment of experiences gathered prior to cocaine administration in rats

Cocaine can induce severe neurobehavioral changes, among others, the ones involved in learning and memory processes. It is known that during drug consumption, cocaine-associated memory and learning processes take place. However, much less is known about the effects of this drug upon the mechanisms involved in forgetting.The present report focuses on the mechanisms by which cocaine affects memory consolidation of experiences acquired prior to drug administration. We also study the involvement of hippocampus in these processes, with special interest on the role of Nuclear factor kappa B (NF-κB), N-methyl-D-aspartate glutamate receptor 2B (GluN2B), and their relationship with other proteins, such as cyclic AMP response element binding protein (CREB). For this purpose, we developed a rat experimental model of chronic cocaine administration in which spatial memory and the expression or activity of several proteins in the hippocampus were assessed after 36 days of drug administration. We report an impairment in memory acquisition of experiences gathered prior to cocaine administration, associated to an increase in GluN2B expression in the hippocampus. We also demonstrate a decrease in NF-κB activity, as well as in the expression of the active form of CREB, confirming the role of these transcription factors in the cocaine-induced memory impairment.