26 research outputs found

    Going one step further: towards cognitively enhanced problem-solving teaming agents

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    Operating current advanced production systems, including Cyber-Physical Systems, often requires profound programming skills and configuration knowledge, creating a disconnect between human cognition and system operations. To address this, we suggest developing cognitive algorithms that can simulate and anticipate teaming partners' cognitive processes, enhancing and smoothing collaboration in problem-solving processes. Our proposed solution entails creating a cognitive system that minimizes human cognitive load and stress by developing models reflecting humans individual problem-solving capabilities and potential cognitive states. Further, we aim to devise algorithms that simulate individual decision processes and virtual bargaining procedures that anticipate actions, adjusting the system’s behavior towards efficient goal-oriented outcomes. Future steps include the development of benchmark sets tailored for specific use cases and human-system interactions. We plan to refine and test algorithms for detecting and inferring cognitive states of human partners. This process requires incorporating theoretical approaches and adapting existing algorithms to simulate and predict human cognitive processes of problem-solving with regards to cognitive states. The objective is to develop cognitive and computational models that enable production systems to become equal team members alongside humans in diverse scenarios, paving the way for more efficient, effective goal-oriented solutions

    Loss of CDKL5 Causes Synaptic GABAergic Defects That Can Be Restored with the Neuroactive Steroid Pregnenolone-Methyl-Ether

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    : CDKL5 deficiency disorder (CDD) is an X-linked neurodevelopmental disorder characterised by early-onset drug-resistant epilepsy and impaired cognitive and motor skills. CDD is caused by mutations in cyclin-dependent kinase-like 5 (CDKL5), which plays a well-known role in regulating excitatory neurotransmission, while its effect on neuronal inhibition has been poorly investigated. We explored the potential role of CDKL5 in the inhibitory compartment in Cdkl5-KO male mice and primary hippocampal neurons and found that CDKL5 interacts with gephyrin and collybistin, two crucial organisers of the inhibitory postsynaptic sites. Through molecular and electrophysiological approaches, we demonstrated that CDKL5 loss causes a reduced number of gephyrin puncta and surface exposed γ2 subunit-containing GABAA receptors, impacting the frequency of miniature inhibitory postsynaptic currents, which we ascribe to a postsynaptic function of CDKL5. In line with previous data showing that CDKL5 loss impacts microtubule (MT) dynamics, we showed that treatment with pregnenolone-methyl-ether (PME), which promotes MT dynamics, rescues the above defects. The impact of CDKL5 deficiency on inhibitory neurotransmission might explain the presence of drug-resistant epilepsy and cognitive defects in CDD patients. Moreover, our results may pave the way for drug-based therapies that could bypass the need for CDKL5 and provide effective therapeutic strategies for CDD patients

    Voluminous gastric fibrosarcoma in a 75-year-old patient

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    Research into New Molecular Mechanisms in Thrombotic Diseases Paves the Way for Innovative Therapeutic Approaches

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    Thrombosis is a multifaceted process involving various molecular components, including the coagulation cascade, platelet activation, platelet endothelial interaction, anticoagulant signaling pathways, inflammatory mediators, genetic factors and the involvement of various cells such as endothelial cells, platelets and leukocytes. A comprehensive understanding of the molecular signaling pathways and cell interactions that play a role in thrombosis is essential for the development of precise therapeutic strategies for the treatment and prevention of thrombotic diseases. Ongoing research in this field is constantly uncovering new molecular players and pathways that offer opportunities for more precise interventions in the clinical setting. These molecular insights into thrombosis form the basis for the development of targeted therapeutic approaches for the treatment and prevention of thrombotic disease. The aim of this review is to provide an overview of the pathogenesis of thrombosis and to explore new therapeutic options

    Genetic immunization with the immunodominant antigen P48 of <i>Mycoplasma agalactiae</i> stimulates a mixed adaptive immune response in BALBc mice

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    A DNA vaccine against contagious agalactia was developed for the first time, encoding the P48 of Mycoplasma agalactiae. Specific immune responses elicited in BALB/c mice were evaluated. Both total IgG and IgG1 were detected in mice vaccinated with pVAX1/P48. Proliferation of mononuclear cells of the spleen, levels of gamma interferon, interleukin-12, and interleukin-2 mRNAs were enhanced in immunized animals. Results indicate that pVAX1/P48 vaccination induced both Th1 and Th2 immune responses. Nucleic acid immunization could be a new strategy against M. agalactiae infections and may be potentially used to develop vaccines for other Mycoplasma diseases

    Combination anticancer endowed with antitumor activity, comprising alkaloids of chelidonium majus

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    The invention relates to a combination having antitumor activity, wherein an agent having antineoplastic activity, such as gemcitabine or temozolomide, is associated with an alkaloid of Chelidonium majus (C. majus), such as berbenne, chelidonine or protopine
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