The outbreak of coronavirus disease 2019 (COVID-19) has been spreading rapidly in China and the Chinese government took a series of policies to control the epidemic. Studies found that severe COVID-19 is characterized by pneumonia, lymphopenia, exhausted lymphocytes and a cytokine storm. Studies have showen that SARS-CoV2 has significant genomic similarity to the severe acute respiratory syndrome (SARS-CoV), which was a pandemic in 2002. More importantly, some diligent measures were used to limit its spread according to the evidence of hospital spread. Therefore, the Public Health Emergency of International Concern (PHEIC) has been established by the World Health Organization (WHO) with strategic objectives for public health to curtail its impact on global health and economy. The purpose of this paper is to review the transmission patterns of the three pneumonia: SARS-CoV2, SARS-CoV, and MERS-CoV. We compare the new characteristics of COVID-19 with those of SARS-CoV and MERS-CoV.
Long non-coding RNAs (lncRNAs) are the key components of non-coding RNAs (ncRNAs) with a length of 200 nucleotides. They are transcribed from the so-called "dark matter" of the genome. Increasing evidence have shown that lncRNAs play an important role in the pathophysiology of human diseases, particularly in the development and progression of tumors. Linc-ROR, as a new intergenic non-protein coding RNA, has been considered to be a pivotal regulatory factor that affects the occurrence and development of human tumors, including breast cancer (BC), colorectal cancer (CRC), pancreatic cancer (PC), hepatocellular carcinoma (HCC), and so on. Dysregulation of Linc-ROR has been closely related to advanced clinicopathological factors predicting a poor prognosis. Because linc-ROR can regulate cell proliferation, apoptosis, migration, and invasion, it can thus be used as a potential biomarker for patients with tumors and has potential clinical significance as a therapeutic target. This article reviewed the role of linc-ROR in the development of tumors, its related molecular mechanisms, and clinical values.
Activation of quiescent hepatic stellate cells (HSCs) is the major event in liver fibrosis, along with enhancement of cell proliferation and overproduction of extracellular matrix.Recent findings suggest that senescence of activated HSCs might limit the development of liver fibrosis. The p53, a guardian of the genome is associated with liver fibrosis, has been shown to regulate HSCs senescence. In this study, we report that microRNA-145 (miR-145) and p53 were downregulated in vivo and in vitro, concomitant with the enhanced expression of zinc finger E-box binding homeobox 2 (ZEB2). In addition, overexpression of miR-145 and p53 led to upregulation of the number of senescence-associated βgalactosidase-positive HSCs and the expression of senescence markers p16 and p21, along with the reduced abundance of HSC activation markers α-smooth muscle actin and type I collagen in activated HSCs. Furthermore, silencing of ZEB2 promoted senescence of activated HSCs. Moreover, we also demonstrated that miR-145 specifically targeted the 3′-untranslated regions of ZEB2. In vitro promoter regulation studies show that ZEB2 could bind to the E-box of the p53 promoter as well as inhibit its promoter activity and thus suppress the expression of p53, which in turn repressed activated HSCs senescence.Taken together, our results describe a novel miR-145-ZEB2-p53 regulatory line might participate in the senescence of activated HSCs and might carry potential therapeutic targets for restraining liver fibrosis.
Extracellular vesicles (EVs) are small membranous vesicles secreted from normal, diseased, and transformed cells in vitro and in vivo. EVs have been found to play a critical role in cell-to-cell communication by transferring non-coding RNAs (ncRNAs) including microRNAs (miRNAs), long ncRNAs (lncRNAs) and so on. Emerging evidence shows that transferring biological information through EVs to neighboring cells in intercellular communication not only keep physiological functions, but also participate in the pathogenesis of liver diseases. Liver diseases often promote release of EVs and/or in different cargo sorting into these EVs. Either of these modifications can promote disease pathogenesis. Given this fact, EV-associated ncRNAs, such as miR-192, miR-122 and lncRNA-ROR and so on, can serve as new diagnostic biomarkers and new therapeutic targets for liver disease, because altered EV-associated ncRNAs may reflect the underlying liver disease condition. In this review, we focus on understanding the emerging role of EV-associated ncRNAs in viral hepatitis, liver fibrosis, alcoholic hepatitis (AH), non-alcoholic steatohepatitis (NASH) and hepatocellular carcinoma (HCC) and discuss their utility in biomarker discovery and therapeutics. A better understanding of this multifaceted pattern of communication between different type cells in liver may contribute to developing novel approaches for personalized diagnostics and therapeutics.
Takotsubo syndrome (TTS) can develop after liver transplant (LT), but its predisposing factors are poorly understood. In this study, we aimed to determine if perioperative factors were associated with posttransplant TTS. Adult patients who underwent primary LT between 2006 and 2018 were included. Patients with and without TTS were identified and matched by propensity scores. Of 2181 LT patients, 38 developed postoperative TTS with a mean left ventricular ejection fraction of 25.5% (±7.8%). Multivariable logistic regression revealed two preoperative risk factors (alcoholic cirrhosis and model for end-stage liver disease-sodium scores) for TTS. Post-propensity match analyses showed that TTS patients had significantly higher doses of epinephrine and lower doses of fentanyl during LT compared with non-TTS patients. A higher dose of epinephrine and a lower dose of fentanyl was associated with a higher predicted probability of TTS. All TTS patients had full recovery of cardiac function and had comparable 1-year survival. In conclusion, TTS occurred at a rate of 1.7% after LT and was associated with two pretransplant risk factors. The higher doses of epinephrine and lower doses of fentanyl administered during LT were associated with posttransplant TTS. More studies on the relationship between intraoperative medications and TTS are warranted.
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