5 research outputs found

    Properties of Vanadium Bronzes Synthesized by Different Methods

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    Paroxysmal Atrial Fibrillation: Dynamics of The Main Antioxidant Enzymes - Superoxide Dismutase and Catalase

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    Abstract INTRODUCTION: Researchers have a particularly strong interest in the mechanisms implicated in the clinical manifestation of atrial fibrillation. OBJECTIVE: To examine dynamically the activity of the antioxidant enzymes, su-peroxide dismutase and catalase in patients with paroxysmal atrial fibrillation (duration ⋋ 48 hours). MATERIALS AND METHODS: The studied parameters were examined in the erythrocytes of 51 patients (59.84 ± 1.60, 26 men) immediately after their hospitalization, at 24 hours and 28 days after restoration of sinus rhythm. 52 controls (59.50 ± 1.46, 26 men) were also included, none of which had a history of arrhythmia. Propafenone was used to manage the rhythm abnormality. The enzyme activity was determined by a spectrophotometric method. RESULTS: The average duration of atrial fibrillation episodes until the time of hospitalization was 8.14 hours (from 2 to 24 hours). During patient hospitalization the activity of superoxide dismutase and catalase was considerably higher compared to that of the controls (8.46 ± 0.26 vs 5.81 ± 0.14 U/mg Hb; 7.36 ± 0.25 vs 4.76 ± 0.12 E240/min/mg Hb; P ⋋ 0.001). This difference was maintained 24 hours after the rhythm regularization (7.19 ± 0.25 vs 5.81 ± 0.14 U/mg Hb, p ⋋ 0.001; 5.30 ± 0.21 vs 4.76 ± 0.12 E240/min/mg Hb, p ⋋ 0.05). Twenty-eight days after the restoration of sinus rhythm, the activity of catalase remained increased (5.11 ± 0.08 vs 4.76 ± 0.12 E240/min/mg Hb, p ⋋ 0.05). CONCLUSION: The paroxysmal atrial fibrillation in our study was characterized with significantly increased activity of superoxide dismutase and catalase even in the early hours of clinical manifestation of the disorder, which then slowly decreased with the restoration of sinus rhythm. Therefore, we can conclude that changes in oxidative status are closely related to the disease and are probably a part of the intimate mechanisms related to its initiation and clinical course.</jats:p

    Paroxysmal Atrial Fibrillation: Dynamics of The Main Antioxidant Enzymes - Superoxide Dismutase and Catalase

    No full text
    INTRODUCTION: Researchers have a particularly strong interest in the mechanisms implicated in the clinical manifestation of atrial fibrillation

    Loss of DOT1L disrupts neuronal transcription and leads to a neurodevelopmental disorder

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    Individuals with monoallelic gain-of-function variants in the histone lysine methyltransferase DOT1L display global developmental delay and varying congenital anomalies. However, the impact of monoallelic loss of DOT1L remains unclear. Here, we sought to define the effects of partial DOT1L loss by applying bulk and single-nucleus RNA-sequencing, ChIP-sequencing, imaging, multielectrode array recordings, and behavioral analysis of zebrafish and multiple mouse models. We present a cohort of 16 individuals (12 females, 4 males) with neurodevelopmental disorders and monoallelic DOT1L variants, including a frameshift deletion, an in-frame deletion, a nonsense, and missense variants clustered in the catalytic domain. We demonstrate that specific variants cause loss of methyltransferase activity. In primary cortical neurons, Dot1l knockdown disrupts transcription of synaptic genes, neuron branching, expression of a synaptic protein, and neuronal activity. Further in the cortex of heterozygous Dot1l mice, Dot1l loss causes sex-specific transcriptional responses and H3K79me2 depletion, including within down-regulated genes. Lastly using both zebrafish and mouse models, we found behavioral disruptions that include developmental deficits and sex-specific social behavioral changes. Overall, we define how DOT1L loss leads to neurological dysfunction by demonstrating that partial Dot1l loss impacts neuronal transcription, neuron morphology, and behavior across multiple models and systems.</p
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