Diagnostic and therapeutic performances of three score-based Thyroid Imaging Reporting and Data Systems after application of equal size thresholds.

Background: The aim of this study was to explore the diagnostic and therapeutic performances of the artificial intelligence (AI), American College of Radiology (ACR), and Kwak Thyroid Imaging Reporting and Data Systems (TIRADSs) using the size thresholds for fine needle aspiration (FNA) and follow-up defined in the ACR TIRADS. Methods: This retrospective study included 3,833 consecutive thyroid nodules identified in 2,590 patients from January 2010 to August 2017. Ultrasound (US) features were reviewed using the 2017 white paper of the ACR TIRADS. US categories were assigned according to the ACR/AI and Kwak TIRADS. We applied the thresholds for FNA and follow-up defined in the ACR TIRADS to the Kwak TIRADS. The diagnostic and therapeutic performances were calculated and compared using the McNemar or DeLong methods. Results: The AI TIRADS had higher specificity, accuracy, and area under the curve (AUC) than did the ACR and Kwak TIRADS (specificity: 64.6% vs. 57.4% and 52.69%; accuracy: 78.5% vs. 75.4% and 73.0%; AUC: 88.2% vs. 86.6% and 86.0%; all P values <0.05). Meanwhile, the AI TIRADS had a lower FNA rate (FNAR), unnecessary FNA rate (UFR), and follow-up rate (FUR) than did the ACR and Kwak TIRADS using the size thresholds of the ACR TIRADS (specificity: 30.9% vs. 34.4% and 36.9%; accuracy: 41.1% vs. 47.8% and 48.7%; AUC: 34.2% vs. 37.7% and 41.0%; all P values <0.05). In addition, the Kwak TIRADS incorporating the size thresholds of the ACR TIRADS was almost similar to the ACR TIRADS in diagnostic and therapeutical performance. Conclusions: The ACR TIRADS can be simplified, which potentially enhances its diagnostic and therapeutic performance. The method of score-based TIRADS (counting in the Kwak TIRADS and weighting in the ACR and AI TIRADS) might not determine the diagnostic and therapeutic performances of the TIRADS. Thus, we propose choosing a straightforward and practical TIRADS in daily practice.

EPO promotes axonal sprouting via upregulating GDF10.

Erythropoietin (EPO) has an exact neuroprotective effect on stroke. However, it remains unknown whether it participates in axonal sprouting after neuron damage. Growth and differentiation factor 10 (GDF10) has been shown to be a trigger of axonal sprouting after stroke. Hence, it was hypothesized that EPO promotes axonal sprouting mainly through GDF10. In the present in vitro experiment, it was found that EPO could promote axonal sprouting and GDF10 expression in a dose-dependent manner. The knockdown of GDF10 using siRNA abolished the effect of EPO-mediated axonal sprouting, indicating that GDF10 is the executor of EPO-mediated axonal sprouting. The treatment of neurons with nuclear factor-kappaB (NF-κB) inhibitor JSH-23 could inhibit the accumulation of NF-κB phospho-p65 (p-p65) in the nucleus, the upregualtion of GDF10 and extending of axonal length. Furthermore, the addition of Janus kinase 2 (JAK2) inhibitor CEP-33779 or phosphoinositide 3-kinase (PI3K) inhibitor LY294002 to the culture medium also blocked the nuclear translocation of p-p65, the expression of GDF10, and axonal sprouting, suggesting that EPO induces axonal sprouting via activating cellular JAK2 and PI3K signaling. Impeding JAK2 signaling with CEP-33779 can suppress the phosphorylation of PI3K, and this confirms that the upstream of PI3K signaling is JAK2. These present results provide a novel insight into the role of EPO and the molecular mechanism of axonal sprouting, which is beneficial for the development of novel approaches for neurological recovery after brain injury, including stroke.

Significance of ABCA1 in human carotid atherosclerotic plaques.

The ATP-binding cassette transporter A1 (ABCA1) is an important effector in the regulation of cholesterol efflux from cells. In this study, we assessed the role of ABCA1 in human carotid atherosclerotic plaques (CAPs). We found that ABCA1 and retinoid X receptor α (RXRα) mRNAs were significantly increased in the atherosclerotic plaques compared to control arteries. The increased ABCA1 mRNA correlated with that of RXRα in plaques. According to the modified American Heart Association plaque classification, atherosclerotic specimens were assigned to three grades, and ABCA1 and RXRα mRNA levels were compared across plaques of different grades. Resultantly, plaques of grade II and III exhibited higher mRNA levels than grade I, but there was no difference in mRNA levels between plaques of grade II and III. By contrast, ABCA1 and RXRα protein levels were notably reduced in plaques relative to control tissues. Similarly, plaques of grade II and III exhibited lower ABCA1 and RXRα protein levels than grade I, and there was no difference in protein levels between plaques of grade II and III. Our findings suggest that decreased ABCA1 protein plays a key role in the pathogenesis of CAP; the regulation of ABCA1 may be mediated by RXRα and ABCA1 mRNA levels may serve as an indicator for plaque stability.