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Herein we report Lewis acid HfCl4-catalyzed [4 + 2] cycloaddition between ß,γ-unsaturated α-keto esters and various symmetric or unsymmetric alkynes, giving the desired polysubstituted 4H-pyrans in up to 98% yield and with excellent regioselectivity (>99:1) via a vinyl carbocation under mild conditions.
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Switchable enantioselectivity was uncovered in the enantioselective catalytic conjugate addition of ß,γ-unsaturated α-keto esters with terminal alkynes to the chiral Lewis acid complex of In(BF4)3 and chiral phosphoric acid.
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(1) Background: It is well-known that long non-coding RNAs (lncRNAs) and N7-methylguanosine (m7G) contribute to hepatocellular carcinoma (HCC) progression. However, it remains unclear whether lncRNAs regulating m7G modification could predict HCC prognosis. Thus, we sought to explore the prognostic implications of m7G-related lncRNAs in HCC patients. (2) Methods: Prognostic M7G-related lncRNAs obtained from The Cancer Genome Atlas (TCGA) database were screened by co-expression analysis and univariate Cox regression analysis. Next, the m7G-related lncRNA signature (m7GRLSig) was conducted by Least absolute shrinkage and selection operator (LASSO) Cox regression and multivariate Cox regression analysis. Kaplan-Meier analysis and time-dependent receiver operating characteristics (ROC) assessed the prognostic abilities of our signature. Univariate and multivariate Cox regression, nomogram, and principal component analysis (PCA) were conducted to evaluate our signature. Subsequently, we investigated the role of m7GRLSig on the immune landscape and sensitivity to drugs in HCC patients. The potential function of lncRNAs obtained from the prognostic signature was explored by in vitro experiments. (3) Results: A novel m7GRLSig was identified using seven meaningful lncRNA (ZFPM2-AS1, AC092171.2, PIK3CD-AS2, NRAV, CASC19, HPN-AS1, AC022613.1). The m7GLPSig exhibited worse survival in the high-risk group and served as an independent prognostic factor. The m7GRLSig stratification was sensitive in assessing the immune landscape and sensitivity to drugs between the high-risk and low-risk groups. Finally, in vitro experiments confirmed that the knockdown of NRAV was accompanied by the downregulation of METTL1 during HCC progression. (4) Conclusions: The m7G-related signature is a potential predictor of HCC prognosis and contributes to individualize the effective drug treatment of HCC.
Assuntos
Carcinoma Hepatocelular , Neoplasias Hepáticas , RNA Longo não Codificante , Humanos , Carcinoma Hepatocelular/genética , RNA Longo não Codificante/genética , Neoplasias Hepáticas/genética , PrognósticoRESUMO
OBJECTIVES: The aim of this study was to evaluate the risk factors for hyperglycemia development after a first episode of acute pancreatitis (AP). METHODS: Three hundred and ten patients treated for AP were retrospectively evaluated. Hyperglycemia was determined by fasting blood glucose. All data were collected from the medical records room database and a follow-up telephone call. RESULTS: The incidence rate of hyperglycemia was obviously increased 5 years after the event. Hazard ratios (HRs) of developing hyperglycemia in patients with hyperlipidemia, fatty liver, and hypertension were 2.52 (P < 0.001), 1.87 (P = 0.01), and 1.78 (P = 0.017), respectively. Patients of biliary origin that underwent endoscopic retrograde cholangiopancreatography presented a 4.62-fold greater risk than those managed conservatively. Other risk factors were random blood glucose greater than 8.33 mmol/L (HR, 4.19; P < 0.001), lactate dehydrogenase greater than 350 U/L (HR, 1.99; P = 0.017), calcium less than 1.75 mmol/L (HR, 3.86; P = 0.004), and elevated creatine kinase (HR, 2.74; P = 0.001). Patients with AB blood type showed 2.92-fold greater risk compared with those with O blood type. Among them, hyperlipidemia and hyperglycemia on admission were the only independent risk factors (both P < 0.05). CONCLUSIONS: Hyperlipidemia, fatty liver, hypertension, endoscopic retrograde cholangiopancreatography treatment, acute hyperglycemia, elevated lactate dehydrogenase and creatine kinase, decreased calcium, and AB blood type were risk factors for hyperglycemia development after AP.