Inflammaging is a potential risk factor for cardiovascular diseases. It results in the development of thrombosis and atherosclerosis. The accumulation of senescent cells in vessels causes vascular inflammaging and contributes to plaque formation and rupture. In addition to being an acquired risk factor for cardiovascular diseases, ethanol can induce inflammation and senescence, both of which have been implicated in cardiovascular diseases. In the current study, we used colchicine to abate the cellular damaging effects of ethanol on endothelial cells. Colchicine prevented senescence and averted oxidative stress in endothelial cells exposed to ethanol. It lowered the relative protein expression of aging and senescence marker P21 and restored expression of the DNA repair proteins KU70/KU80. Colchicine inhibited the activation of nuclear factor kappa B (NFκ-B) and mitogen activated protein kinases (MAPKs) in ethanol-treated endothelial cells. It reduced ethanol-induced senescence-associated secretory phenotype. In summary, we show that colchicine ameliorated the ethanol-caused molecular events, resulting in attenuated senescence and senescence-associated secretory phenotype in endothelial cells.
Robust preclinical models are inevitable for researchers to unravel pathomechanisms of subarachnoidal hemorrhage (SAH). For the mouse perforation model of SAH, the goal of this meta-review was the determination of variances in mortality, SAH severity grade, and vasospasm, and their experimental moderators, as many researchers are facing with incomparable results. We searched on the databases PubMed, Embase, and Web of Science for articles describing in vivo experiments using the SAH perforation mouse model and measuring mortality, SAH grade, and/or vasospasm. After screening, 42 articles (total of 1964 mice) were included into systematic review and meta-analysis. Certain model characteristics were insufficiently reported, e.g., perforation location (not reported in six articles), filament (material (n = 15) and tip texture (n = 25)), mouse age (n = 14), and weight (n = 10). Used injective anesthetics and location of perforation showed large variation. In a random-effects meta-analysis, the overall animal mortality following SAH was 21.3% [95% CI: 17.5%, 25.7%] and increased with longer observational periods. Filament material significantly correlated with animal mortality (p = 0.024) after exclusion of hyperacute studies (time after SAH induction < 24 h). Reported mean SAH grade was 10.7 [9.6, 11.7] on the scale of Sugawara (J Neurosci Methods 167:327–34, 2008). Furthermore, mean diameter of large cerebral arteries after SAH was reduced by 27.6% compared to sham-operated non-SAH mice. Uniforming standards of experimental procedures and their reporting are indispensable to increase overall comparability.
Background: Angiocentric glioma (AG) is an extremely rare intracranial tumor that was first described in 2005 and identified as a special type of intracranial tumor in 2007 by the WHO, which mainly affects children and young adolescents. Epilepsy is the main presentation; therefore, it was recognized as a seizure-related tumor in the past. Here, we report a case of AG with acute intracerebral hemorrhage (ICH) as the first symptom who never had a seizure onset. Case Description: A 3-year-old girl with the right limb weakness was admitted to our hospital 4 h after onset in 2018. Computed tomography showed a hematoma of about 20 ml accompanied by a hyper/iso-dense spheroid lesion located in the sub-cortex of the left parietal lobe. Magnetic resonance image (MRI) showed signs of hypointense signal in T1, T2, and fluid-attenuated inversion recovery sequence, distinct enhancement of this tumefactive lesion in the contrast-enhanced sequence. Thus, the admission diagnosis was neoplasm with acute ICH. A gross total resection of the tumor was achieved by parietal craniotomy. The histopathological diagnosis was AG. No signs showed tumor recurrence after 36 months of follow-up. Conclusion: This is the sole case of AGs with acute intracranial hemorrhage as the first symptom without any kind of epilepsy by far. This case had unique MRI signs that were different from the previous description. This case enriches the clinical and radiological manifestations of AG and reveals that further investigations are needed to further understand AG.
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