Furthermore, high-doses of TGF-β1 suppressed collagen II, but enhanced collagen I, TIMP-3, MMP-13, ALK1/5 and Smad1/2/3/5/8 expression. ALK5 inhibition induced the suppression of Smad2/3 and aggravated high-dose TGF-β1-induced NPC degeneration, as shown by the reduction in collagen II and increase in collagen I, TIMP-3 and MMP-13. By contrast, ALK1 inhibition resulted in Smad1/5/8 suppression and alleviated high-dose TGF-β1-induced NPC degeneration. Taken together, it was concluded that high-doses of TGF-β1 contributed to the degeneration of NPCs via the upregulation of ALK1 and Smad1/5/8.The stability of carotid artery plaque serves a key role in the occurrence of stroke. The present study was based on the recruitment of patients with acute ischemic cerebrovascular disease. High-resolution magnetic resonance imaging (HR-MRI) was used to identify the nature of carotid artery plaque, and the results were then used to manage the high-risk group of stroke. The patients were divided equally into a symptomatic group (36 cases) and an asymptomatic group (36 cases). According to the degree of carotid artery stenosis, the patients were divided into mild, moderate and severe stenosis groups, each group comprising 12 patients, and HR-MRI was performed. The proportion of patients with vulnerable plaque in the symptomatic group was higher compared with that in the asymptomatic group (P less then 0.05). The more severe the stenosis, the higher the proportion of vulnerable plaque that was identified (P less then 0.05). Compared with carotid ultrasound, HR-MRI was indicated to have the capability to both identify and quantify the different components in the plaque, allowing an assessment of its properties. In conclusion, the present study demonstrated that carotid HR-MRI is able to distinguish and quantify the different components of plaque, which may prove to be helpful for the hierarchical management of a population at high risk of stroke.The aim of the present study was to explore how dynamic contrast-enhanced magnetic resonance imaging (DCE-MRI) may differentiate hepatocellular carcinoma (HCC) from hepatic metastasis of rectal cancer (HMRC) by extracting pharmacokinetic parameters and radiomic features. A total of 75 patients, including 41 cases with HCC and 34 cases with HMRC, underwent DCE-MRI examination. Dual-input two-compartment extended Tofts tracer kinetic model attached to a specialized image post-processing software package from OmniKinetics; GE Healthcare was used to calculate the values of the pharmacokinetic parameters and radiomic features, which were extracted from the lesions at the same region of interest. Binimetinib MEK inhibitor These values were evaluated using Student’s t-test and receiver operating characteristic curves, and discriminant models were built to differentiate between HCC and HRMC. The results identified statistically significant differences in the values of the pharmacokinetic parameters hepatic perfusion index (HPI), endothelial tths improved the diagnostic efficacy. A discriminant model based on radiomic features further enhanced the identification of HCC and HMRC.The metastatic behavior of hepatocellular carcinoma (HCC) is one of the key factors that leads to poor prognosis. The aim of the current study was to determine the changes in metastasis and the proliferation potential of bone marrow mesenchymal stem cells (BMSCs) in high metastatic potential hepatocellular carcinoma (MHCC97-H) following gene silencing. The osteopontin (OPN) and transforming growth factor-β (TGFβ1 ) genes, which are associated with metastasis and tumor proliferation, were silenced in MHCC97-H cells. Transwell assays were used to evaluate the migration of MHCC97-H cells in vitro. Additionally, a murine model of MHCC97-H lung metastasis was established. Following OPN and TGFβ1 silencing, the migration of MHCC97-H cells was significantly reduced following BMSC intervention (P0.05). The metastasis and proliferation potential of MHCC97-H following BMSC intervention were significantly reduced in vitro and in vivo, especially in the TGFβ1-silenced group. The decrease in the metastatic potential in gene-silenced MHCC97-H cells was not associated with integrin αvβ3 expression. Therefore, OPN and TGFβ1 may be potential targets for HCC treatment, and TGFβ1 may have a higher therapeutic potential for BMSC intervention.Status epilepticus (SE) is a neurological disorder associated with high morbidity and mortality rates, and is often difficult to treat. Moreover, the underlying mechanism of SE remains unknown. The lithium-pilocarpine model is a validated animal model that can reproduce the main clinical and neuropathological features of SE. In the present study, this SE model was utilized and SE was successfully established in rats, as determined by the corresponding epileptic electroencephalogram. Histology, immunohistochemistry, western blot analysis and co-immunoprecipitation were used to detect the phosphorylation (p-) of AKT substrate of 40 kDa (PRAS40), the combination of p-PRAS40 and 14-3-3 protein and the activation of the PI3K/mTOR signaling pathway in SE. In addition, the present study analyzed the dynamics of the expression of autophagy-associated factors in the hippocampus after SE induction, and the influence of suppressing the p- of PRAS40 on the autophagy process was detected in the pathogenesis of SE. The results indicated that increased p-PRAS40 expression could activate the mTOR pathway to decrease the level of autophagy. However, inhibition of the mTOR signaling pathway promoted autophagy flux. These results may provide further understanding of p-PRAS40 functions in SE.Long non-coding RNAs (lncRNAs) serve a crucial role in every aspect of cell biological functions as well as in a variety of diseases, including cardiovascular disease, cancer and nervous system disease. However, the differential expression profiles of lncRNAs in Marfan syndrome (MFS) have not been reported. The aim of the present study was to identify potential target genes behind the pathogenesis of MFS by analyzing microarray profiles of lncRNA in aortic tissues from individuals with MFS and normal aortas (NA). The differentially expressed lncRNA profiles between MFS (n=3) and NA (n=4) tissues were analyzed using microarrays. Bioinformatics analyses were used to further investigate the candidate lncRNAs. Reverse transcription-quantitative (RT-qPCR) was applied to validate the results. In total, the present study identified 294 lncRNAs (245 upregulated and 49 downregulated) and 644 mRNAs (455 upregulated and 189 downregulated) which were differential expressed between MFS and NA tissues (fold change ≥1.5; P less then 0.