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Cardiovascular disease (CVD) is the leading cause of death in the United States. Damage in the cardiovascular system can be due to environmental exposure, trauma, drug toxicity, or numerous other factors. As a result, cardiac tissue and vasculature undergo structural changes and display diminished function.

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Tumor necrosis factor-α (TNF-α) induces a multitude of actions and consequences in bone and cartilage resorption and immune response augmentation. In this research, we aimed to investigate the effects of TNF-α on osteogenesis parameters in newborn mice. Experimental research was conducted on 42 pregnant mice, dividing into seven groups as follows: control (no injection), vehicle 1 (PBS injection on 7-9th pregnancy days (PD)), vehicle 2 (PBS injection during pregnancy), experimental 1 (injection of 10 ng/kg of TNF-α on 7-9th PD), experimental 2 (injection of 100 ng/kg of TNF-α on 7-9th PD), experimental 3 (injection of 10 ng/kg of TNF-α during pregnancy) and experimental 4 (injection of 100 ng/kg of TNF-α during pregnancy).

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Background: Cell therapy demonstrates promising potential as a substitute therapeutic approach for liver cirrhosis. We have developed a strategy to effectively expand murine and human hepatocyte-derived liver progenitor-like cells (HepLPCs) in vitro. The primary objective of the present study was to apply HepLPCs to the treatment of liver cirrhosis and to elucidate the underlying mechanisms responsible for their therapeutic efficacy.

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Hyperalgesic priming is a model system that has been widely used to understand plasticity in painful stimulus-detecting sensory neurons, called nociceptors. A key feature of this model system is that following priming, stimuli that do not normally cause hyperalgesia now readily provoke this state. We hypothesized that hyperalgesic priming occurs because of reorganization of translation of mRNA in nociceptors.

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SYNGAP1 is a Ras GTPase-activating protein that plays a crucial role during brain development and in synaptic plasticity. Sporadic heterozygous mutations in SYNGAP1 affect social and emotional behaviour observed in intellectual disability (ID) and autism spectrum disorder (ASD). Although neurophysiological deficits have been extensively studied, the epigenetic landscape of SYNGAP1 mutation-mediated intellectual disability is unexplored.

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