Background Cerebral venous sinus thrombosis (CVST) is a rare neurovascular disorder with highly variable manifestations and clinical courses. Animal models properly matched to the clinical form of CVST are necessary for elucidating the pathophysiology of the disease. In this study, we aimed to establish a rat model that accurately recapitulates the clinical features of CVST in human patients. Methods This study consisted of a clinical analysis and animal experiments. Clinical data for two centres obtained between January 2016 and May 2021 were collected and analysed retrospectively. In addition, a Sprague–Dawley rat model of CVST was established by inserting a water-swellable rubber device into the superior sagittal sinus, following which imaging, histological, haematological, and behavioural tests were used to investigate pathophysiological changes. Principal component analysis and hierarchical clustering heatmaps were used to evaluate the similarity between the animal models and human patients. Results The imaging results revealed the possibility of vasogenic oedema in animal models. Haematological analysis indicated an inflammatory and hypercoagulable state. These findings were mostly matched with the retrospective clinical data. Pathological and serological tests further revealed brain parenchymal damage related to CVST in animal models. Conclusions We successfully established a stable and reproducible rat model of CVST. The high similarity between clinical patients and animal models was verified via cluster analysis. This model may be useful for the study of CVST pathophysiology and potential therapies.
The flame retardant tri (1, 3-dichloro-2-propyl) phosphate (TDCIPP) is widely present in environmental media and organisms. People have paid much attention to the growth and developmental toxicity of TDCIPP, but there is little information about its cardiotoxicity and potential mechanisms. In this study, marine medaka ( Oryzias melastigma ) embryos were exposed to TDCIPP solutions (0, 0.05, 0.5, 5, and 50 μg/L) for 21 days to investigate the adverse effects of TDCIPP on cardiac development. The results showed that TDCIPP exposure altered the heart rate at different stages of embryonic development. In addition, 50 μg/L TDCIPP resulted in increased sinus venosus (SV)–bulbus arteriosus (BA) distance, pericardial cysts, and cardiac linearization in newly hatched fish. During embryonic development, the expression level of key genes regulating cardiac development is disturbed. The early stage of cardiac development is the sensitive window period for the toxic effects of TDCIPP. Oxidative stress was observed in newly hatched juveniles, but no significant lipid peroxidation damage was observed. In addition, vitellogenin (VTG) levels in juvenile fish were significantly reduced. Our results show that TDCIPP exposure induces cardiotoxicity in marine medaka embryos, which is induced in the early stages and promotes heart defects by amplifying inflammatory responses at a later stage.
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