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Archer Tobiasen posted an update 6 months ago
Background Clinical symptoms of multiple sclerosis (MS) are variable and may include cognitive impairment, which can be assessed with the verbal fluency test (VFT). This test is evaluated by counting words spoken during a 2-min period, which is not a functional approach. Ojbective. The objectives of this observational study were to 1) determine new parameters that reflect communication and cognitive functions in persons with multiple sclerosis (PwMS) considering the evaluation of real-time word production in the VFT; 2) compare the results with those of a control group; and 3) evaluate the impact of including errors. Methods A phonological fluency test (“letter P”) and a semantic fluency test (“animals”) were used. The real-time word production was recorded. The main variables studied were the total number of words, first word delay, moment of inflection of the curve corresponding to the change in the cognitive process, speed of word production before inflection, and maximum delay between 2 consecutive words. These variables were studied by taking into account or not errors. Results We included 68 PwMS and 33 healthy controls. VFT results were impaired in PwMS. The total number of words, first word delay, speed before inflection, and maximum delay were relevant to the study of phonologic fluency. For studying semantic fluency, the total number of words, first word delay, speed before inflection, and inflection time of the curve seemed relevant. Taking into account errors was significant only for total number of words. Conclusion Taking into account errors in evaluating real-time word production in PwMS is of interest only for the total number of words performed but has no impact on the variables studied. These variables should be used to quantitatively evaluate verbal fluency with the objective of evaluating functionally relevant parameters (communication).A fundamental shortcoming in the current treatment of schizophrenia is the lack of valid criteria to predict who will respond to antipsychotic treatment. Cirtuvivint The identification of blood-based biological markers of the therapeutic response would enable clinicians to identify the subgroup of patients in whom conventional antipsychotic treatment is ineffective and offer alternative treatments. As part of the Optimisation of Treatment and Management of Schizophrenia in Europe (OPTiMiSE) programme, we conducted an RNA-Seq analysis on 188 subjects with first episode psychosis, all of whom were subsequently treated with amisulpride for 4 weeks. We compared gene expression on total RNA from patients’ blood before and after treatment and identified 32 genes for which the expression changed after treatment in good responders only. These findings were replicated in an independent sample of 24 patients with first episode psychosis. Six genes showed a significant difference in expression level between good and poor responders before starting treatment, allowing to predict treatment outcome with a predictive value of 93.8% when combined with clinical features. Collectively, these findings identified new mechanisms to explain symptom improvement after amisulpride medication and highlight the potential of combining gene expression profiling with clinical data to predict treatment response in first episode psychoses.The network architecture of the human brain contributes in shaping neural activity, influencing cognitive and behavioral processes. The availability of neuroimaging data across the lifespan allows us to monitor how this architecture reorganizes, influenced by processes like learning, adaptation, maturation, and senescence. Changing patterns in brain connectivity can be analyzed with the tools of network science, which can be used to reveal organizational principles such as modular network topology. The identification of network modules is fundamental, as they parse the brain into coherent sub-systems and allow for both functional integration and segregation among different brain areas. In this work we examined the brain’s modular organization by developing an ensemble-based multilayer network approach, allowing us to link changes of structural connectivity patterns to development and aging. We show that modular structure exhibits both linear and nonlinear age-related trends. In the early and late lifespan, communities are more modular, and we track the origins of this high modularity to two different substrates in brain connectivity, linked to the number and the weights of the intra-clusters edges. We also demonstrate that aging leads to a progressive and increasing reconfiguration of modules and a redistribution across hemispheres. Finally, we identify those brain regions that most contribute to network reconfiguration and those that remain more stable across the lifespan.The damaging effects of obesity extend to multiple pre-existing tissue/organs. However, the influence of this condition on key components (inflammation and angiogenesis) of fibrovascular connective proliferating tissue, essential in repair processes, has been neglected. Our objective in this study was to investigate whether obesity would influence inflammatory-angiogenesis induced by synthetic matrix of polyether-polyurethane implanted subcutaneously in high-fat-fed obese C57/BL6 mice. Fourteen days after implantation, the inflammatory and angiogenic components of the newly formed tissue intra-implant were evaluated. The pro-inflammatory enzyme activities, myeloperoxidase (MPO) and N-acetyl-β-D-glucosaminidase (NAG), the levels of TNF-α, CXCL1/KC and CCL2 and NF-κB transcription factor were examined. Angiogenesis was determined by morphometric analysis of implant blood vessels, intra-implant levels of hemoglobin content, VEGF levels, and western blot for VEGFR2. All inflammatory and angiogenic markers were increased in the implants of obese mice compared with their non-obese counterparts. Similarly, activation of the NF-κB pathway and phosphorylation of VEGFR2 were higher in implants of obese mice (1.60 ± 0.28 Np65/Cp65; 0.96 ± 0.08 p-VEGFR2/VEGFR2-T) compared with implants of non-obese animals (1.40 ± 0.14; 0.49 ± 0.08). These observations suggest that obesity exerts critical role in sponge-induced inflammatory-angiogenesis, possibly by activating fibrovascular components in the inflamed microenvironment. Thus, this pathological condition causes damage not only to pre-existing tissues/organs but also to newly formed proliferating fibrovascular tissue. This is relevant to the development of therapeutic approaches to improve healing processes in patients with obesity.
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