Refractory status epilepticus (RSE) is a condition with serious mortality and morbidity rate, resistant to benzodiazepine and second-line antiepileptic drugs. This study aimed to electrophysiologically investigate the combination of NMDA receptor antagonist ketamine and GABAergic agent propofol in an RSE model induced by lithium-pilocarpine in male Sprague-Dawley rats. Seventy-two male Sprague-Dawley rats were divided into nine groups.
View Article and Find Full Text PDFChronic liver disease (CLD) represents a significant global health burden, with hepatic steatosis-associated disorders-such as metabolic dysfunction-associated steatohepatitis (MASH), alcoholic liver disease, and hepatitis C virus infection-being major contributors. Recent genome-wide association studies have identified the rs72613567:TA variant in the 17-beta-hydroxysteroid dehydrogenase 13 () gene as a protective factor against the development and progression of these conditions. In this review, we summarized the current evidence surrounding the rs72613567 variant, aiming to elucidate its impact on CLD risk and outcomes, and to explore the potential mechanisms behind its hepatoprotective effects.
View Article and Find Full Text PDFBackground And Aim: It is reported that miRNAs play an important role in hepatocellular carcinogenesis and may serve as non-invasive biomarkers for hepatocellular carcinoma (HCC). MiR-4510 and miR-146b-5p expression levels have been found to be associated with HCC. However, their associations with hepatitis B virus (HBV)-related HCC (HBV-HCC) are yet to be explored.
View Article and Find Full Text PDFBackground And Aims: Progression to hepatocellular carcinoma (HCC) is restricted by viral suppression in chronic hepatitis B (CHB); however, some patients still progress despite antiviral therapy. Presence of single nucleotide polymorphisms (SNPs) such as PNPLA3 rs738409 and TM6SF2 rs58542926 are associated with the development and progression of steatotic liver disease to HCC, whereas a splice variant in HSD17B13 rs72613567:TA has been shown to be protective. We investigated the role of these SNPs in the development or prognosis of HCC in pure CHB etiology, in the absence of hepatic steatosis, remains unknown.
View Article and Find Full Text PDF