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Sökning: WFRF:(Gil Jeovanis) > (2023)

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1.
  • Gil, Jeovanis, et al. (författare)
  • Improved Melatonin Dissolution Properties : A Way Forward for Treating Children with Sleep Disorders
  • 2023
  • Ingår i: Dissolution Technologies. - 1521-298X. ; 30:2, s. 66-71
  • Tidskriftsartikel (refereegranskat)abstract
    • Sleep problems, in particular the difficulty in initiating and maintaining sleep are important comorbidities in children and adolescents with attention deficit hyperactivity disorder (ADHD), accompanied by a range of negative consequences for both patients and their caregivers. Melatonin, a naturally occurring hormone that is important for coordinating the body's sleep-wake cycle, has been used to treat insomnia in children with ADHD. This study compares the dissolution properties of two melatonin tablets (1 and 5 mg Mellozzan and Melatonin AGB). Results showed that Mellozzan dissolved rapidly (90% within 5 minutes) in all pH levels tested, whereas Melatonin AGB dissolved slower (60% within 30 minutes). The fast dissolution properties of melatonin observed in Mellozzan indicates that this formulation is preferable for the treatment of children where the dissolution step is critical to reach the desired clinical effect.
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2.
  • Pomeshchik, Yuriy, et al. (författare)
  • Proteomic analysis across patient iPSC-based models and human post-mortem hippocampal tissue reveals early cellular dysfunction and progression of Alzheimer's disease pathogenesis
  • 2023
  • Ingår i: Acta Neuropathologica Communications. - 2051-5960. ; 11
  • Tidskriftsartikel (refereegranskat)abstract
    • The hippocampus is a primary region affected in Alzheimer's disease (AD). Because AD postmortem brain tissue is not available prior to symptomatic stage, we lack understanding of early cellular pathogenic mechanisms. To address this issue, we examined the cellular origin and progression of AD pathogenesis by comparing patient-based model systems including iPSC-derived brain cells transplanted into the mouse brain hippocampus. Proteomic analysis of the graft enabled the identification of pathways and network dysfunction in AD patient brain cells, associated with increased levels of Aβ-42 and β-sheet structures. Interestingly, the host cells surrounding the AD graft also presented alterations in cellular biological pathways. Furthermore, proteomic analysis across human iPSC-based models and human post-mortem hippocampal tissue projected coherent longitudinal cellular changes indicative of early to end stage AD cellular pathogenesis. Our data showcase patient-based models to study the cell autonomous origin and progression of AD pathogenesis.
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